Constipation & Plant-Based Diets

Studies suggest 1 2 that around 20% of people in Westernised countries suffer from constipation. That’s a lot of unpleasant and largely unnecessary toilet trouble by any standards. But is there a simple, drug-free remedy? You can bet your beans and greens there is!

Fibre, fibre, fibre

The most common lifestyle choice associated with the development of constipation is eating a low-fibre diet.

It still comes as something as a surprise just how many people are completely unaware that fibre can only be found in foods derived from plants – fruit and veg, beans, whole grains, etc – and that there is ZERO fibre in meat, dairy products, and eggs.

The average daily fibre intake in the UK is 17.2 grams/day for women and 20.1 grams/day for men, with a government recommendation of a minimum of 30 grams/day 3 . In the US, the recommendations vary from 19-38 grams/day, whilst US fibre intake is even less than the UK, at around 16 grams/day 4 5 . And, because these are averages, it means there are plenty of people eating considerably less than this.

A previous blog 6 discussed fibre in more detail, and pointed out that eating as much as 100 grams of fibre daily was quite normal in earlier human evolution.

In those countries where traditional diets contain much more fibre, it’s no surprise to find that constipation is much less common. But how can we know that it’s the fibre that’s making so much difference? Well, studies have looked at the changes that occur when such countries adopt the modern Western diet, which is much lower in fibre content. And what they’ve found is that constipation prevalence increases. 7 8

Constipation by country

There’s a very detailed list of reported constipation cases available at 9 , but the following selective chart from a 2008 study 10  shows a common finding: namely, that women tend to suffer more than men.

Key: United States (US), United Kingdom (UK), France (FR), Germany (GE), Italy (IT), Brazil (BR) and South Korea (SK).

Problems arising from constipation

There are a number of complications which may arise from constipation 11 12 , including:

  • haemorrhoids (from “straining at the stool”)
  • anal fissures
  • rectal prolapse
  • faecal impaction (also called malignant constipation), which may lead to:
    • bowel obstruction
    • nausea
    • vomiting
    • tender abdomen
  • encopresis (where soft stool from the small intestine bypasses the impacted faecal mass in the colon)

How to prevent and alleviate constipation

It’s pretty obvious that the most sensible and natural method will involve increasing fibre content in the diet.

In children, studies show 13 14 that a lower intake of dietary fibre differentiates children with chronic constipation from those who have regular bowel movements. It’s so sad that children have to undergo such suffering simply because their parents and carers fail (whether through ignorance or conscious choice) to feed them a diet that maintains their gut health. Of course, it’s not just the problem of constipation that’s at issue here; maintaining a healthy gut microbiome from early life is vital for overall health through childhood and into old age 15 16 17 18 . And it’s such an obvious yet largely unappreciated fact 19 that our GI tract (along with all the trillions of essential bacteria, fungi and other microbes therein) is best maintained by a whole food plant-based diet rather than a diet of processed and/or animal foods.

As would be expected, therefore, additional studies show that increasing dietary fibre improves constipation and significantly reduces the need for laxatives in all societal groups:

  • children 20
  • young adults 21
  • elderly people 22 , and
  • post-surgery patients 23

When fibre supplementation may be necessary

Naturally, the first and best option is to increase the consumption of high-fibre foods. This is because, by eating whole plant foods, we don’t just facilitate easier gut transit, but the fibre itself and the natural healthy bacteria included with plants act as probiotics and prebiotics for our gut bacteria, and a variety of plants provides a vast array of minerals, vitamins, and an almost inestimable number of beneficial phytochemicals.

However, there are situations where chewing away on fibrous plant food is not an option, and so, in the following cases, fibre supplements may be the best option:

  • individuals lacking teeth (edentulism)
  • patients who can’t swallow easily or at all (dysphagia)

Prescribing laxatives is a very general knee-jerk reaction of medical professionals. They seem to choose this because they don’t appear to believe their patients have the wherewithal to significantly alter their diets. However, suggesting fibre supplements, in the case of the above two conditions, or changing to a high-fibre diet, in the case of most patients, is far more successful than merely pouring laxatives down your throat while still eating the same constipating diet. When the second best alternative (fibre supplements) are offered, evidence suggests 24  that around 60% of constipated patients can dispense with the laxatives they had been previously taking.

Different types of fibre supplements

The following have been shown to be effective for constipation relief:

  • psyllium (Metamucil) 25 (although prunes have been shown 26  to be more effective than psyllium)
  • methylcellulose (Citrucel) 27
  • Japanese konjac root (glucomannan) 28

But, I repeat, the first and best option is to transition to a plant-based diet (ideally non-SOS WFPB) unless, of course, you have no teeth or cannot swallow easily. And, even the latter two cases, I would suspect that there may be some way found to ensure whole plant foods are eaten, even if they have to be pulped or liquidised to some extent. I have some personal experience of this situation, since my father developed COPD 29 and dysphagia. Being crippled and having to be cared for my my mother, she was told that he would only ever be able to eat pureed food. However, she found that with some careful selection of foods, he was able to eat “solid” food almost until the time of his eventual death.

Dehydration & constipation

Even mild dehydration is a very common factor in cases of constipation 30 31 . This has also been found 20  to be the case in young constipated children. And it’s easy to understand why this is the case, and how it links inextricably with diet, when you realise that whole plant foods contain loads of water, while processed and animal foods can contain considerably less – and also usually contain loads of dehydrating salt.

Becoming dehydrated, without being aware of it, is much easier and more widespread than most of us realise. This can be seen from a US study 32 which found a shocking 75% of US citizens were chronically dehydrated.

In patients with functional chronic constipation, it’s been shown 33  that combining fibre and fluid (25 grams and 1.5-2.0 litres, respectively) on a daily basis was more effective for constipation relief than simply taking fibre alone.

It’s no surprise, then, that Dr Greger includes water consumption as one of the essential items in his Daily Dozen list 34 , stating that “…authorities from Europe, the U.S. Institute of Medicine, and the World Health Organization recommend between 2 to 2.7 liters of water a day for women. That’s 8 to 11 cups a day for women, and 10 to 15 cups a day for men. Now but that’s water from all sources–not just beverages–and we get about a liter from food and the water our body actually makes. So these translate into a recommendation for women to drink 4 to 7 cups of water a day, and men 6 to 11 cups, assuming only moderate physical activity at moderate ambient temperatures.” 35 .

Constipation & cow’s milk

Many children with chronic constipation are found 36 to be allergic to cow’s milk, manifesting IgE antibodies 37 to cow’s milk antigens38 . It’s always worthwhile for parents to ensure that any difficulties occurring during potty training are not associated with constipation resulting from the child drinking cow’s milk.

This is no insignificant matter, since consumption of cow’s milk has been found 39 to be significantly higher in infants and children with constipation and anal fissure than in those without these disorders.

And it gets even worse. Colonoscopies revealed 40  that around 50% of constipated, cow’s milk-allergic children and adolescents had lymphoid nodular hyperplasia 41 , compared with 20% of controls. The same study also found that around 33% of all cow’s milk-allergic individuals had a significantly higher number of intraepithelial T cells 42 , indicating an enhancement of local immune responses against food antigens. Another study of children with lymphoid modular hyperplasia found 43  that in 43 of the 52 individuals a diagnosis of cow’s milk or multiple food hypersensitivity was made.

Such activation of the immune system is known 44 to affect gastric motility 45 , thus indicating a likely role for an immune response to food antigens in cases of constipation.

Cow’s milk or soy milk?

Cutting out cow’s milk totally, in the diets of those children with cow’s milk sensitivity and constipation, has been shown 46  to result in significant improvement in up to 66% of cases.

In a small-scale study 47 of children with constipation, 100% of the participants had full resolution of chronic functional constipation when soy milk was used as a replacement for cow’s milk.

A further study found 48 that when cow’s milk was reintroduced, constipation returned within 5-10 days.

Previous blogs 49 50 have discussed in much more detail the range of health issues associated with cow’s milk. In basic terms, for all humans, irrespective of age, there’s absolutely no nutritional need for “baby calf growth fluid” 51 to be included in the diet. And, for a significant number of both children and adults who experience constipation, it would seem a sensible plan to try cutting out cow’s milk completely to see whether relief of symptoms follows.

Final thoughts

So, getting lots of fibre, drinking plenty of fluids and avoiding cow’s milk seem to be the major routes towards non-drug prevention and treatment of constipation in all age groups. One area we haven’t covered is regular physical exercise, which, counter to popular belief, does not have any overwhelming study evidence to support its value for constipation treatment or avoidance. Some studies consider that it can be an important adjunct for males 52 and females 53  of all age groups in the prevention and treatment of constipation. However, other studies, including the following 2017 French study, question whether increasing exercise per se has any positive effect:

The benefi[t] of increasing water intake or daily physical exercise in the treatment of chronic constipation have a lack of evidence, except specific situations such as elderly, hospitalized, institutionalized, dehydrated people or people consuming fluids less than 500mL/day. Change in environmental defecation conditions or bowel habits are probably anecdotal recommendations.” 54

Yet other authorities consider 55 that, in some cases of particularly intense exercise, constipation can be worsened. More research is needed on which level of activity (stationary yoga movements, gentle walking or marathon running, for instance) has what effect on constipation.

Whilst lack of exercise is particularly important as we age and run the risk of becoming too sedentary 56 , the increasing rates of childhood obesity – and the associated reduction in physical exercise – are reported by some studies as revealing a worrying increase in cases of constipation and other GI health concerns 57 58 .

My personal experience is that the effects of exercise appear to be determined, at least to some extent, on the quality of diet you are consuming. If you’re already eating a low-fibre diet and then exercise, I have no doubt that it might lead to increased constipation; however, when a high-fibre diet is your norm, exercise may not have the same effect. A comparison study would be of interest in this respect.

What all studies agree on, however, is that the main and overreaching factor of importance in avoiding and treating constipation is fibre, fibre and more fibre.

So, in conclusion, whilst it’s easy to say that best means of achieving healthy GI tract activity is to follow a varied WFPB diet, keep hydrated and ensure that you get plenty of daily exercise, when we have had a lifetime of practising ingrained and unquestioned habits, it can be really difficult to make such lifestyle and dietary changes.  However, ensuring that our children do not fall into bad habits will both protect them and encourage us to embrace healthier practices ourselves.

References & Notes

  1. Higgins PD, Johanson JF. Epidemiology of constipation in North America: a systematic review . Am J Gastroenterol . 2004; 99: 750–759. []
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  3. British Nutrition Foundation: Dietary fibre. []
  4. Hoy MK, Goldman JD. Fiber intake of the U.S. population: What We Eat in America, NHANES 2009–2010. United States Department of Agriculture website. []
  5. U.S. Department of Agriculture and Agricultural Research Service. What We Eat in America: Dietary Fiber (g): Usual Intakes from Food and Water, 2003-2006, Compared to Adequate Intakes. National Health and Nutrition Examination Survey (NHANES) 2003-2006. United States Department of Agriculture website. []
  6. Fibre! Fibre! Fibre! []
  7. Yang XJ et al: Epidemiological study: Correlation between diet habits and constipation among elderly in Beijing region. World J Gastroenterol 22:8806, 2016 []
  8. Holmboe-Ottesen G, Wandel M. Changes in dietary habits after migration and consequences for health: a focus on South Asians in Europe. Food Nutr Res . 2012;56. []
  9. by Country for Constipation []
  10. AP&T. A multinational survey of prevalence and patterns of laxative use among adults with self‐defined constipation. A. WALD C. SCARPIGNATO S. MUELLER‐LISSNER M. A. KAMM U. HINKEL I. HELFRICH C. SCHUIJT K. G. MANDEL. First published: 01 September 2008 []
  11. Walia R, Mahajan L, Steffen R (October 2009). “Recent advances in chronic constipation”. Curr Opin Pediatr. 21 (5): 661–6. []
  12. McCallum IJ, Ong S, Mercer-Jones M (2009). “Chronic constipation in adults”. BMJ. 338: b831. []
  13. Kranz S et al: What do we know about dietary fiber intake in children and health? The effects of fiber intake on constipation, obesity, and diabetes in children. Adv Nutr 3:47, 2012. []
  14. Castillejo G et al: A controlled, randomized, double-blind trial to evaluate the effect of a supplement of cocoa husk that is rich in dietary fiber on colonic transit in constipated pediatric patients. Pediatrics 118:e641, 2006. []
  15. Gut Microbiota & Depression []
  16. Fibromyalgia, Probiotics & Gut Microbiota []
  17. Physical Activity for Disease Prevention & Healthy Gut Microbiome []
  18. Multiple Sclerosis (MS), Serotonin & Gut Microbiota []
  19. Two Types of Gut Bacteria: Plant Eaters’ & Meat Eaters’ []
  20. Castillejo G et al: A controlled, randomized, double-blind trial to evaluate the effect of a supplement of cocoa husk that is rich in dietary fiber on colonic transit in constipated pediatric patients. Pediatrics 118:e641, 2006 [] []
  21. Woo HI et al: A Controlled, Randomized, Double-blind Trial to Evaluate the Effect of Vegetables and Whole Grain Powder That Is Rich in Dietary Fibers on Bowel Functions and Defecation in Constipated Young Adults. J Cancer Prev 20:64, 2015 []
  22. Howard LV, West D, Ossip-Klein DJ: Chronic constipation management for institutionalized older adults. Geriatr Nurs 21:78, 2000 Mar-Apr []
  23. Griffenberg L et al: The effect of dietary fiber on bowel function following radical hysterectomy: a randomized trial. Gynecol Oncol 66:417, 1997 []
  24. Sturtzel B et al: Use of fiber instead of laxative treatment in a geriatric hospital to improve the wellbeing of seniors. J Nutr Health Aging 13:136, 2009 []
  25. Ramkumar D, Rao SS: Efficacy and safety of traditional medical therapies for chronic constipation: systematic review. Am J Gastroenterol 100:936, 2005 []
  26. Prunes vs. Metamucil vs. Vegan Diet. Michael Greger M.D. FACLM March 15th, 2013 Volume 12 []
  27. Mounsey A, Raleigh M, Wilson A: Management of Constipation in Older Adults. Am Fam Physician 92:500, 2015 []
  28. Yen CH et al: Long-term supplementation of isomalto-oligosaccharides improved colonic microflora profile, bowel function, and blood cholesterol levels in constipated elderly people–a placebo-controlled, diet-controlled trial. Nutrition 27:445, 2011 []
  29. Chronic Obstructive Pulmonary Disease (COPD) is an umbrella term used to describe progressive lung diseases including emphysema, chronic bronchitis, and refractory (non-reversible) asthma. This disease is characterised by increasing breathlessness. []
  30. Eur J Clin Nutr. 2003 Dec;57 Suppl 2:S88-95. Mild dehydration: a risk factor of constipation? Arnaud MJ []
  31. Murakami K et al: Association between dietary fiber, water and magnesium intake and functional constipation among young Japanese women. Eur J Clin Nutr 61:616, 2007 []
  32. Survey of 3003 Americans, Nutrition Information Center, New York Hospital-Cornell Medical Center. April 14, 1998. []
  33. Anti M et al: Water supplementation enhances the effect of high-fiber diet on stool frequency and laxative consumption in adult patients with functional constipation. Hepatogastroenterology 45:727, 1998 May-Jun []
  34. Dr. Greger’s Daily Dozen Checklist. Michael Greger M.D. FACLM September 11th, 2017 Volume 38 []
  35. How Many Glasses of Water Should We Drink a Day? Michael Greger M.D. FACLM May 25th, 2015 Volume 24 []
  36. Cow’s milk protein allergy in children: identification and treatment. The Pharmaceutical Journal15 MAY 2018. By Hetal Dhruve, Joanne Walsh, David Mass, Adam Fox. []
  37. IgE antibodies: If you have an allergy, your immune system overreacts to an allergen by producing antibodies called Immunoglobulin E (IgE). These antibodies travel to cells that release chemicals, causing an allergic reaction. This reaction usually causes symptoms in the nose, lungs, throat, or on the skin. []
  38. Antigens are toxins or other foreign substances which induce an immune response in the body, especially the production of antibodies. []
  39. Andiran F, Dayi S, Mete E: Cows milk consumption in constipation and anal fissure in infants and young children. J Paediatr Child Health 39:329, 2003 []
  40. Turunen S, Karttunen TJ, Kokkonen J: Lymphoid nodular hyperplasia and cow’s milk hypersensitivity in children with chronic constipation. J Pediatr 145:606, 2004 []
  41. Lymphoid nodular hyperplasia (LNH) generally presents as an asymptomatic disease, but it may cause gastrointestinal symptoms like abdominal pain, chronic diarrhoea, bleeding or intestinal obstruction. []
  42. Intraepithelial T cells (IETs), residing at the epithelial barrier in the gastrointestinal tract, are an epitome of tissue-resident T cells. Tissue-resident T cells are long-lived, nonrecirculating T cells that provide rapid immune responses independent of peripheral T cell recruitment. []
  43. Clin Gastroenterol Hepatol. 2007 Mar;5(3):361-6. Colonic lymphoid nodular hyperplasia in children: relationship to food hypersensitivity. Iacono G, Ravelli A, Di Prima L, Scalici C, Bolognini S, Chiappa S, Pirrone G, Licastri G, Carroccio A. []
  44. Hermann GE, Tovar CA, Rogers RC: Induction of endogenous tumor necrosis factor-alpha: suppression of centrally stimulated gastric motility. Am J Physiol 276:R59, 1999 []
  45. Gastric Motility: contractions of gastric smooth muscle that serves two basic functions: ingested food is crushed, ground and mixed, liquefying it to form what is called chyme. Chyme is then forced through the pyloric canal into the small intestine, a process called gastric emptying. []
  46. Carroccio A et al: Chronic constipation and food intolerance: a model of proctitis causing constipation. Scand J Gastroenterol 40:33, 2005 []
  47. Crowley ET et al: Does milk cause constipation? A crossover dietary trial. Nutrients 5:253, 2013 []
  48. Iacono G et al: Intolerance of cow’s milk and chronic constipation in children. N Engl J Med 339:1100, 1998 []
  49. If You Want Enough Calcium, Forget Milk []
  50. Cow’s Milk – But It Looks So Innocent… []
  51. ‘Cow’s milk’ as baby calf growth fluid: video with Michael Klaper. []
  52. Harvard Men’s Health Watch. Chronic constipation: A strain for men. Published: September, 2008 []
  53. Diabetes Metab Syndr Obes. 2017; 10: 513–519. Effects of a proposed physical activity and diet control to manage constipation in middle-aged obese women. Sayed A Tantawy, Dalia M Kamel, Walid Kamal Abdelbasset, and Hany M Elgohary []
  54. Presse Med. 2017 . Jan;46(1):23-30. doi: 10.1016/j.lpm.2016.03.019. Epub 2017 Jan 5. [Diet and lifestyle rules in chronic constipation in adults: From fantasy to reality…]. [Article in French]. Fathallah N, Bouchard D, de Parades V. []
  55. Exercise Causes Constipation! By Ashok T Jaisinghani, October 4, 2016 in Diet & holistic health []
  56. NIH: Concerned About Constipation? []
  57. PLoS One. 2014; 9(2): e90193. Physical Activity and Constipation in Hong Kong Adolescents. Rong Huang, Sai-Yin Ho, Wing-Sze Lo, and Tai-Hing Lam []
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How Can Parents Get Toddlers To Eat Healthily?

There are a number of methods to ensure that toddlers eat healthily, and there’s probably been no other time in human history when it’s been more important to do so. Child obesity and all its associated metabolic diseases are hitting children at ever younger ages 1 2 3 . Whilst it’s so easy to blame Big Business and national governments, the primary responsibility for ensuring our children grown up healthy is now, as it always has been, mostly in the hands of their own parents and carers.

Definition of terms

Although not written in stone, the stages of early childhood are conventionally understood as the following:

  • newborn – between 0 and 2 months
  • infant – between 2 and 12 months
  • toddler – between 12 months and 4 years

Getting it right from the start

The most important time to ensure the development of healthy eating habits is arguably during the early weaning process – that is, the period when the baby is transitioning from mother’s breast milk to solid food. I am taking for granted that we would all agree the newborn’s ideal first nutrition (for around the first 6 months) should always be exclusively mother’s breast milk whenever possible. All the evidence points in this direction 4 5 6 .

Bad habits are hard to break

Between around 6 and 12 months of age, the infant will be introduced to “solid” food. It’s during this stage that major mistakes can be made, and bad eating habits (food high in calories and low in nutrients) can be set in motion.

If, however, appropriate food (high in nutrients and sufficient in calories for growth) is introduced, ingrained bad habits within the infant and toddler stages can be avoided, with the remaining years of childhood (and probably adulthood) thus standing a much better chance of being free from the need to put endless effort into undoing such habits – yo-yo dieting, continual fighting to escape the pleasure trap, with all its tempting and addictive bliss points 7.

The importance of good example

Whether or not less-favourable eating habits have been established, parents and carers need to ensure that they act as good examples. This means:

  • eating a healthy and varied balance of foods themselves
  • eating at regular times
  • sharing meals – making each meal a special family event, rather than simply eating separately in front of the TV
  • encouraging toddlers to eat 3 meals a day plus 2 healthy snacks. This can avoid those hunger pangs that can result in unhealthy ‘grazing’ between meals and then overeating during meals

Children who grow up seeing their parents and carers forever on diets or bingeing on unhealthy foods is not something that will act as a good example.

One recent story I heard was of a nutritionist who was asked to intervene in a family where the young child refused to eat anything that even appeared to be a vegetable or a fruit, preferring instead to eat a diet existing more or less solely of sweets, crisps and cakes. The nutritionist advised that containers of bite-sized carrots and celery be left around the kitchen for the child to be attracted to eat. The nutritionist then walked past the veg and said something along the lines of “Oh look! How lovely! Carrots. I love them” and then tucked into them with glee. When the father was asked to do the same, as a means of giving positive feedback to the child, he picked up a carrot, bit into it and pulled a face that would have been better suited to a person who had just swallowed a bumble bee. Naturally, the child saw his father’s reaction and the nutritionist could immediately identify the major reason that the child had developed such unhealthy habits.

Toddlers in the kitchen

Even from the youngest age, infants will be influenced by the sorts of foods they encounter. This isn’t just a matter of flavours, but also of smell, texture, colour, and general variety – the colours of the rainbow.

The relationship parents and carers have to matters relating to food preparation itself will have an effect on the growing child. Involving the toddler from an early age in making meals and understanding the nature of different foods can be of great help in ensuring the child grows up with knowledge about and control over dietary matters.

Any parent will find that toddlers simply love experimenting with the selection and preparation of food. This playful experience is a great way for them to try different foods in the kitchen. It, along with meal times, should be a fun way to spend time with the family. The idea of simply placing already-prepared meals in front of a toddler may be attractive in terms of saving preparation time; however, doing so would tend to miss the exciting and productive times when he or she (or a group of toddlers, be they friends or siblings) could be involved in handling, selecting, chopping, peeling, and even cooking (with careful supervision, of course).

I remember that when I was young I asked my mother what tongue was – you know, those greyish-red slices of meat that bear no resemblance to that huge, dripping muscular organ lolling out of the mouths of cows. I’d been eating it for years and it hadn’t dawned on me that what we called slices of tongue was actually part of a dead animal. I mean, they called candyfloss candyfloss, but you don’t floss candy with it! Anyway, once I discovered what it was, I never touched it again. Had I been responsible for cutting it out of the mouth of the dead cow and then slicing and boiling it, perhaps I would have developed an aversion to it at an even earlier age. Who knows?


Toddler or parent temptation?

Avoiding the temptation to give in to a toddler’s potential demands for sweets and treats is increasingly difficult for parents, what with the ubiquitous advertising campaigns and availability in toddler-height shelves in most shops these days. Even when it comes to those special times, it’s still so important to avoid making unhealthy junk foods a treat or a central part of festivals, birthdays and other celebrations.

If a toddler grows up thinking that a real treat is enjoying a healthy salad rather than being thrown a bag of prawn cocktail crisps or a bag of Haribo Starmix, it’s a pretty good indication that something has been done right!

Of course, parents themselves have to engage in the same fight with sweet and junky temptations that they may well have had since their own childhoods. In this case, fighting one’s own natural desires for sweet indulgence is a preface to allowing one’s children to grow up with more freedom from cravings and learned preferences associated with such toxic foods.

And it hardly needs saying saying that using foods in any way to establish or maintain emotional control is to be avoided. As soon as emotional states (positive or negative) are inextricably linked to food, problems can arise. The art of developing a sense of well-being which is separate from the need for oral satisfaction is something that one would wish all children to learn at an early age. It allows them freedom to seek emotional satisfaction and achievement in other more productive spheres of life.

Eat when hungry

Thus, it’s useful for toddlers to grow up learning that they eat when they are hungry – not when they are forced to do so or because they are bored or depressed.

In any case, toddlers have tiny stomachs which, if filled with unhealthy foods, will leave no room for more essential nutrients. This is where portion control comes into its own. In order to ensure that the toddler does not get used to over-eating, the type and quantity of foods they are presented with should be taken into consideration. Just as there should be no justification for “forcing” an infant or toddler to eat something that he or she does not want to eat, it is equally unhelpful for them to force food down when their body is telling them that they have eaten enough.

Allowing infants and toddlers to exercise some choice in the foods they put into their mouths is advisable – so long as the selection is from healthy and interesting foods. If they don’t want to eat at the moment, fine – be patient and wait until they feel hungry. In the meantime, they can see their parents enjoying the same sorts of food, without having made a big issue of the child’s not eating at that moment. A relaxed atmosphere around the dining table is always likely to produce healthy and easy-going dietary habits in the child.

When hunger hits and ‘seconds’ are required, they should be from a selection of vegetables or fruit. If the toddler wants more immediately after having eaten their meal, it might be a good idea to encourage them to wait for a little while in order to let the food “settle” – allowing leptin to do its job 8 – before they have extra portions.

Learning portion control early in life is a useful means of preventing over-eating in future years. This is not usually a problem, however, with those who eat a non-SOS WFPB diet, since the range of foods within this dietary regime tend to be self-limiting. It’s only when the stomach is filled with high calorie/low nutrient alternatives 9 that over-eating is something that parents should be really concerned about – both for themselves and their children – being that processed foods are carefully manufactured to be addictive “pleasure traps” as they hit those “bliss points” 10 .

Anticipation can be better than participation

Learning ‘satisfaction-delay’ is a really good skill for children to learn young. If a toddler gets what he or she wants immediately upon request, they don’t learn how to delay pleasurable experiences, and learning how to live with the delayed pleasure of eating is a useful skill that spills over into most aspects of child and adult life.

Delaying gratification isn’t a new concept. Back in 300 BC, Aristotle saw that the reason so many people were unhappy was that they confused pleasure for true happiness. True happiness, according to Aristotle, is about developing habits and surrounding yourself with people who grow your soul.” 11

Variety (within reason) matters

Introducing a variety of foods is important and, as stated before, not forcing a child to eat a particular food, if they feel a strong dislike for it, is a sensible move. The chances are that they will change their minds later and try the foods if they see adults enjoying them and not making an issue of them. Patience is the key. This planet of ours grows so many wonderful edible plants that finding alternatives should never be a problem for the attentive parent.

Whilst toddlers are, of course, too young to receive pocket money and run the risk of spending it on sweets etc, any food choices they are able to make at this young age should be from as healthy a range of options as possible. This means keeping only healthy foods in the house and trying to avoid the aisles in supermarkets which draw their attention to unhealthy foods – unfortunately, this is virtually impossible in the modern Western food shopping experience.

Take care with carers

Parents should make their dietary rules very clear to any carers who take responsibility for the toddler. Bad habits learned from carers can cause conflict in the child when they return to their parents and find that they are being told a different story about what dietary habits are or are not acceptable. This applies to both the type and quantity of foods themselves and the regularity and form of dining habits.

Thinking before drinking

In terms of drinks, toddlers should not get used to filling up on sugary drinks. It should go without saying that infants receive their best source of liquids from their mother’s breast milk. Providing drinking fluids during weening is, of course, a natural and essential route, so long as the liquid provided is plain water.

It’s hard to find any authority that would advise parents to give their toddlers fizzy/sugary drinks. The best thing is to avoid all sugary drinks completely so that the child becomes accustomed and perfectly content with simple tap water.

Parents would be wise to do a bit of careful research before deciding to follow the crowd in giving their toddlers cow’s milk. Parents usually feed cow’s milk to their children because they had it themselves and it’s something that is, well, just done! However, much of this is based on an arguably inaccurate belief that cow’s milk is necessary to ensure children get enough calcium 12 . There are some pretty convincing arguments, based on solid research 13 12 , that would caution against feeding cow’s milk to your child, especially when there are plenty of fortified plant milk alternatives 14 to choose from.

It may come as a surprise to some people, but even fruit juices are not an ideal drink 15 , especially if they have added sugar or artificial sweeteners. If, however, they are to be given to toddlers, they should be diluted with water.

Final thoughts

The foregoing is by no means a comprehensive overview of the many ways in which parents can encourage healthy eating habits in their children during the earliest stages of their lives. For my part, I wish my parents had followed even a few of the ideas outlined above. My overly sweet childhood diet resulted in countless rotten teeth and fillings during my adolescent years. This has been accompanied with a life-long struggle against using sweet and fatty junk foods as a reward for a tiring day, a pick-me-up when feeling a little low, and a treat whenever there’s a “y” in the day!

This is why engendering good dietary habits from a young age is so very important. It’s easier to do the right thing when you don’t have to continually undo the wrong.

I wouldn’t wish on anyone a lifetime of being good at bad habits.


  1. Can The UK Government Really Combat Child Obesity? []
  2. England’s Obesity Hotspots []
  3. The State of Childhood Obesity in the US []
  4. Research on Breastfeeding & Breast Milk at the NICHD []
  5. British Nutrition Foundation: SACN’s ‘Feeding in the First Year of Life’. []
  6. NHS: Benefits of Breastfeeding []
  7. Bliss Points, Pleasure Traps & Wholefood Plant-Based Diets. []
  8. Leptin – The “Fat” Hormone? []
  9. Toxic Hunger vs Real Hunger []
  10. Bliss Points, Pleasure Traps & Wholefood Plant-Based Diets []
  11. Psychology Today: The Benefits of Delaying Gratification. Are You Avoiding Pain or Living With Purpose? Dec 26, 2017. []
  12. If You Want Enough Calcium, Forget Milk [] []
  13. Cow’s Milk – But It Looks So Innocent… []
  14. Plant Milks Are Churning Up The Ground []
  15. Fruit Juice by []

Improve Blood Flow By Hanging Upside Down?

It might sound a bit odd, but apparently it’s possible to improve metabolic measures related to blood flow simply by hanging upside down. However, get it wrong and you might end up killing yourself.

It’s well-known that regular aerobic exercise is good for the heart. But various yoga positions also appear to do a similar trick without the need for so much sweating.

One particular yoga pose of specific interest is the upside down position. Of course, as you can see below, there are plenty of different ways of achieving this.

What are the upside down benefits?

A 2011 review 1  into the benefits of yoga in general considered that upside down (or inverted) yoga poses were of benefit to the cardiovascular system:

Inverted poses encourage venous blood flow from the legs and pelvis back to the heart and then pumped through the lungs where it becomes freshly oxygenated. Many studies 2 3 4 show yoga lowers the resting heart rate, increases endurance, and can improve the maximum uptake and utilisation of oxygen during exercise.

There are plenty of yoga websites 5 6 7 8 that give advice on the best way to achieve this inverted pose – variously called supported headstand, sirsasana, inversions, and so forth.

Any yoga’s good yoga

Naturally, this is not the only yoga pose that studies have shown has health benefits. Studies suggest a wide range of benefits, such as:

  • neurological disorders 9 , including:
    • multiple sclerosis 10
    • stroke 11
    • epilepsy 12
    • Parkinson’s disease 13
    • dementia 14
    • Alzheimer’s 15
  • hypertension 16
  • obesity 17
  • diabetes 18
  • depression 19

The list goes on and on…

Dying to be upside down

However, you should be warned that this is not one of those things where a little is good and a lot is even better. Too much inversion can kill 20 .

In 2009, a guy called John Jones, who lived in Utah, died after spending 28 hours stuck upside down in a cave 21 , most likely from asphyxiation.

Upside down lungs

It transpires that our lungs evolved to sit on top of all the other organs for a very good reason. They are such delicate organs that it doesn’t take them long to get squashed by the larger and heavier organs such as the liver and intestines that usually sit below them. 22

This isn’t a problem for sloths, since they have their lungs “taped” to their ribs 23 .

But for us mere humans, having our heads directly underneath our feet for extended periods of time means that the lungs simply can’t absorb enough oxygen given the restricted space they have to work within.

Upside down brain

And it’s not just our lungs that have difficulty. Our bodies are set up to move blood around when we’re upright. Our blood vessels are customised to make sure blood doesn’t pool in our feet. This system is a “one-way street”, since our bodies didn’t evolve to prevent blood from pooling in the brain. This is patently not the case with bats. They have one-way valves in their arteries that prevent blood from flowing backwards. This is why they are able to hang upside down without the blood rushing to their heads 24 .

However, unlike bats, Batman would get into all sorts of vascular trouble (with or without the help of Robin) – ruptured blood vessels and potential brain haemorrhage included.

Upside down heart

And the heart is no lover of too much life down under 25 . It’s thought that heart failure accounts for most upside down fatalities. Just as with the brain, when the heart is above the head, it pumps more slowly and starts to receive more blood than it has the capacity to deal with at any one time. The result is that it begins to have a hard time maintaining blood pressure. Eventually, it will lose its ability to move sufficient blood around to maintain all the body’s essential functions.

Hanging around for too long will eventually kill you – a risk which increases as we age or if we are sick.

Inversion can be torture

It should be remembered that inversion was used as a torture method is ye olde days. It combined pain with a smattering of humiliation. Often the torture of choice for those sinners with unorthodox beliefs, it was used by the Romans with Christians and the Spanish with Jews and Muslims 26 27  . The Japanese even have a word for it – Tsurushi or “reverse hanging” 28 .

Nice to see how relaxed that monk-like executioner appears!

Another thing they used to do was to keep the victim inverted for some time and then make them stand upright again. Apparently, this is very painful as the blood pools to the feet again. Of course, they’re then hung upside down again. This process usually kills them within 8 to 10 hours.

Oh how inventive we humans are…

Final thoughts

It’s probably the case that any exercise is good exercise – whether it’s resistance training with weights, aerobic, or yoga. The important thing is to ensure you get plenty of regular daily exercise – either 90 mins low-moderate intensity (e.g. walking) or 45 mins of high-intensity exercise (e.g cycling, running, or rowing). It’s generally suggested 29 that you can work out your maximum heart rate by simply subtracting your age from 220. Then you can think of low-moderate intensity as being 50 – 70% of the resulting figure, whilst high-intensity would be 70-85%.

Spending a little time upside down appears to be something worth considering – however, some methods of achieving this are better than others…


  1. Int J Yoga. 2011 Jul-Dec; 4(2): 49–54. Exploring the therapeutic effects of yoga and its ability to increase quality of life. Catherine Woodyard. []
  2. Effect of yoga on cardiovascular system in subjects above 40 years. Bharshankar JR, Bharshankar RN, Deshpande VN, Kaore SB, Gosavi GB. Indian J Physiol Pharmacol. 2003 Apr; 47(2):202-6. []
  3. Hatha yoga: improved vital capacity of college students. Birkel DA, Edgren L Altern Ther Health Med. 2000 Nov; 6(6):55-63. []
  4. Effects of Hatha yoga and Omkar meditation on cardiorespiratory performance, psychologic profile, and melatonin secretion. Harinath K, Malhotra AS, Pal K, Prasad R, Kumar R, Kain TC, Rai L, Sawhney RC J Altern Complement Med. 2004 Apr; 10(2):261-8. []
  5. Yoga Journal: Supported Headstand []
  6. Yoga Journal: Everybody Upside-Down []
  7. YouTube video: How to Do a Headstand (Sirsasana) Yoga []
  8. DoYouYoga: 10 Most Popular Yoga Inversions []
  9. J Clin Neurosci. 2017 Sep;43:61-67. doi: 10.1016/j.jocn.2017.05.012. Epub 2017 Jun 7. Evidence based effects of yoga in neurological disorders. Mooventhan A, Nivethitha L. []
  10. PLoS One. 2014 Nov 12;9(11):e112414. doi: 10.1371/journal.pone.0112414. eCollection 2014. Yoga for multiple sclerosis: a systematic review and meta-analysis. Cramer H, Lauche R, Azizi H, Dobos G, Langhorst J. []
  11. Cochrane Database Syst Rev. 2017 Dec 8;12:CD011483. doi: 10.1002/14651858.CD011483.pub2. Yoga for stroke rehabilitation. Lawrence M, Celestino Junior FT, Matozinho HH, Govan L, Booth J, Beecher J. []
  12. Cochrane Database Syst Rev. 2017 Oct 5;10:CD001524. doi: 10.1002/14651858.CD001524.pub3. Yoga for epilepsy. Panebianco M, Sridharan K, Ramaratnam S. []
  13. Trials. 2017 Nov 2;18(1):509. doi: 10.1186/s13063-017-2223-x. The effects of yoga versus stretching and resistance training exercises on psychological distress for people with mild-to-moderate Parkinson’s disease: study prxotocol for a  randomized controlled trial. Kwok JYY, Kwan JCY, Auyeung M, Mok VCT, Chan HYL. []
  14. Int J Geriatr Psychiatry. 2017 Jan;32(1):118. doi: 10.1002/gps.4538. The therapeutic effects of yoga in people with dementia: a systematic review. Du Q, Wei Z. []
  15. Res Gerontol Nurs. 2014 Jul-Aug;7(4):171-7. doi: 10.3928/19404921-20140218-01. Epub 2014 Feb 26. The effect of chair yoga in older adults with moderate and severe Alzheimer’s disease. McCaffrey R, Park J, Newman D, Hagen D. []
  16. Exp Clin Endocrinol Diabetes. 2016 Feb;124(2):65-70. doi: 10.1055/s-0035-1565062. Epub 2015 Nov 17. The Efficacy and Safety of Yoga in Managing Hypertension. Cramer H. []
  17. Prev Med. 2016 Jun;87:213-232. doi: 10.1016/j.ypmed.2016.03.013. Epub 2016 Apr 4. A systematic review and meta-analysis on the effects of yoga on weight-related outcomes. Lauche R, Langhorst J, Lee MS, Dobos G, Cramer H. []
  18. Prev Med. 2017 Dec;105:116-126. doi: 10.1016/j.ypmed.2017.08.017. Epub 2017 Sep 4. The effects of yoga among adults with type 2 diabetes: A systematic review and meta-analysis. Thind H et al. []
  19. Depress Anxiety. 2013 Nov;30(11):1068-83. doi: 10.1002/da.22166. Epub 2013 Aug 6. Yoga for depression: a systematic review and meta-analysis. Cramer H, Lauche R, Langhorst J, Dobos G. []
  20. Quora: How long could a human being survive hanging upside down if they’re being fed, hydrated, etc. Would spending one’s life hanging upside down shorten one’s lifespan? Amandi Dilshara. Oct 24 2019. []
  21. ABC News: Man in Utah Cave Faced Tough Odds, Doctors Say John Jones’ upside down position in the cave left rescue workers little time. By LAUREN COX. Nov. 26, 2009. []
  22. HowStuffWorks: How Your Lungs Work. BY CRAIG FREUDENRICH, PH.D. []
  23. National Geographic: SCIENCE & INNOVATION. To Breathe Upside-Down, Sloths Tape Organs To Their Ribs. BY ED YONG. PUBLISHED APRIL 23, 2014. []
  24. Bat Worlds: Bat Anatomy. Nov 5, 2013. []
  25. How StuffWorks: How Your Heart Works. CARL BIANCO. []
  26. The Marseille Tarot Revealed: A Complete Guide to Symbolism, Meanings & Methods. By Yoav Ben-Dov. []
  27. Bustle: 7 Incredibly Disturbing Execution Methods From The Middle Ages (You Really Should Not Read This) By LARA RUTHERFORD-MORRISON. May 14 2015. []
  28. Wikipedia: Tsurushi. []
  29. Mayo Clinic: Exercise intensity: How to measure it. []

Lose weight Without Exercising or Making Any Dietary Change?

Tackling obesity without exercise or dietary changes? Everyone’s heard of fat tissue (also called adipose tissue), but what about brown adipose tissue (BAT) and “beige” adipose tissue – ever heard of them? Although sounding pretty unappetising,  these adipocytes1 share the unique ability of being able to convert chemical energy into heat and, thereby, play a critical role in promoting something called non-shivering thermogenesis – a little-known process that is central to the human species’ ability to spread across the globe and, as an interesting sideline, can potentially help in weight-loss without even having to lift a single barbell or place a tentative trainer on that running machine gathering dust in your garage. Or is it just too good to be true?

BAT & beige adipocytes

Until relatively recently, the physiological role of BAT and beige adipocyte depots were thought to be limited to small mammals and only relevant to humans when they were neonates (newborn infants). Puppy fat or baby fat was thought to all-but disappear with the passing years into adulthood. However, the discovery that there’s more BAT in adult humans than previously thought, has led to studies which show enthusiasm for BAT’s potential role in treating obesity and other disorders caused by sustained positive energy balance (more calories in than out). Adult humans having more BAT than previously thought was revealed 2 3 during routine scans  (FDG-PET scans4 to detect metastatic cancers. 5  Autopsies were also able to reveal these fat concentrations. 6

Brown & white fat

BAT (often abbreviated to “brown fat”) is found in virtually all mammals, but notably in newborn humans and mammals that hibernate 7 . Of course, the usual white adipose tissue (“white fat”) that we think of when we talk about fat is found in far higher quantities. 8 . The following provides an overview of the differences between the brown and white fat tissue:

The main differences between brown and white fat can be summarised as:

  • white contains a single lipid droplet while brown contains numerous smaller droplets
  • brown contains a much much higher number of (iron-containing) mitochondria – hence the brown (rusty) colour of the tissue 9
  • brown contains more blood capillaries than white – hence a better oxygen supply, more nutrient-provision and the ability to distribute the produced heat throughout the body

Two types of BAT

BAT itself can also broken down into two types which have similar functions but are located in different cell populations within the body: 10

  • brown adipocytes found in comparatively larger separate deposits within the body, and
  • “beige” or “brite” (“brown in white”) adipocytes found interspersed within white adipose tissue and which develop out of white adipocytes under the stimulation of the sympathetic nervous system (SNS) 11
Brown adipose tissue in a woman shown in a PET/CT scan exam.

BAT in infants & adults

BAT in infants eventually “turns into” white fat in adulthood. In infancy, however, it tends to be located in the following “depots” within the body:

  • interscapular 12
  • supraclavicular 13
  • suprarenal 14
  • pericardial 15
  • paraaortic 16
  • around the pancreas, kidney and trachea 17

BAT in adults tend to be located in the following depots:

  • supraclavicular
  • suprarenal
  • paravertebral 18
  • mediastinal 19
  • paraaortic 20

It’s still not absolutely clear whether these adult BAT depots are the “classical” brown or the beige/brite fat. 21 . However, BAT is metabolically active in adult humans 22  and decreases in quantity as we age 23 . Another characteristic of BAT is that it becomes more visible (that is, becomes more metabolically active) with cold exposure – as can be seen by analysing it with PET scans.

BAT & thermoregulation

The primary function of BAT is thermoregulation. That is, ensuring the body remains sufficiently warm in cold environments. It achieves this autonomic heating of the body in two ways: firstly, through shivering thermogenesis (causing muscles to shiver) and, secondly, through non-shivering thermogenesis (as the name suggests – heating the body without shivering) – an adaptive thermogenesis response. The first option, shivering thermogenesis, will certainly warm up the body, but at the expense of using up relatively more precious energy.

However, the unique ability of BAT to convert energy stores (brown fat) into heat (without needing to use energy-sapping shivering) is achieved through a process within BAT mitochondria (the energy-producing cellular power plants). Instead of the usual process, where ATP (the energy molecule) is produced during oxidative phosphorylation, a protein called thermogenin or UCP1 (Uncoupling Protein 1) promotes a proton leak in the inner membrane of the mitochondria, dissociating the oxidative phosphorylation of substrate from the generation of ATP. In essence, this results in an increase in non-shivering thermogenesis, where the metabolic rate increases, and chemical energy is shunted into heat energy that can then spread around the body via the bloodstream.

This means the endothermic organisms (you and me) stand a better chance of survival against unfavourable environmental conditions with the least possible consumption of energy stores 24 . This can be seen in a little more clearly in the following diagram:

Just to be clear, all cells of endotherms are able to give off heat to some degree, particularly when body temperature is below a regulatory threshold; but BAT is highly specialised for this non-shivering thermogenesis. This is largely because of two of the features mentioned above: firstly, each BAT cell has a higher number of mitochondria compared to typical cells and, secondly, these mitochondria have a higher-than-normal concentration of thermogenin (UCP1) in the inner membrane.

Why do newborns have so much BAT?

In newborn infants, BAT comprises around 5% of body mass (located on the upper half of the spine and toward the shoulders). At this age, infants are at a much higher risk of hypothermia than adults. This is largely because of the following:

Infants have:

  • underdeveloped nervous systems that don’t respond quickly and/or appropriately to cold via vasoconstriction (the contraction of blood vessels in and just below the skin)
  • inability to move away from cold materials or air currents or towards warmer materials/environments
  • low amount of musculature and an inability to shiver (shivering thermogenesis)
  • lack of thermal insulation such as subcutaneous fat and fine body hair
  • higher ratio of body surface area (proportional to heat loss) to body volume (proportional to heat production)
  • higher proportional surface area of the head
  • the obvious inability to use adult ways of keeping warm – putting clothes on, exercising, drying their skin, etc

Thus, heat production in BAT provides infants with an alternative means of heat regulation.

Evolutionary advantage of BAT

Mammals (and birds, to some extent) have the unique ability to maintain their core temperature independently of the external environmental temperature. This homeothermic 25 ability has allowed great evolutionary success compared to poikilotherms2627

The main components of this response to temperature are:

  • thermal insulation
  • non-shivering thermogenesis, and
  • shivering thermogenesis 28

From an evolutionary point of view, excess energy expenditure aimed at maintaining core temperature represents a trade-off between survival and the maintenance of energy stores, since energy availability will usually represent a major limiting factor to growth and reproduction. Thus, moving from an insulative response (energy neutral), to a non-shivering and eventually shivering thermogenesis will require a progressively greater dissipation of energy stores, as can be seen in the following chart.

Model of adaptive thermogenesis. As the environmental temperature decreases from thermoneutrality, the adaptive thermogenesis response moves from insulative to non-shivering and eventually shivering thermogenesis. This progression is mirrored by an increase in the energy expenditure required to maintain the core temperature. Green, energy expenditure due to basal metabolic rate; red, expenditure due to adaptive thermogenesis.

Over recent evolutionary development, humans gained the ability to “control” their environment by using clothes and controlling the temperature in their buildings. As a result, cold exposure is a relatively rare condition and, unless acclimatised, individuals would tend to respond by shivering thermogenesis – where heat is a side product of uncontrolled shivering – also known as muscle fasciculation 29

Losing weight & improving health with BAT

Recent discoveries regarding BAT may, it’s claimed, lead to new methods of weight loss, since brown fat (when exposed to cold temperatures) takes calories from normal fat and burns it. As well as this, adaptive (non-shivering) thermogenesis also appears to promote glucose disposal. To test this weight-loss ability of BAT, it would involve exposing subjects to cold temperatures and monitoring whether they do, in fact, lose weight without having to exercise or change dietary patterns. The following is a selection of some BAT studies that throw some light on this subject.

A 1961 study 30 when individuals had prolonged exposure to cold, showed that they became resilient and stopped displaying shivering thermogenesis, indicating that other mechanisms were being recruited.

In 2009, four separate studies 31 32 33 34 indicated clearly that BAT was present in a significant number of adults and that there was a correlation between its presence and activity related to indices of healthy metabolism.

In 2010, a study 35 showed that there was an inverse correlation between BAT activity and between obesity, diabetes and ageing – that is, the more active BAT was, the less obesity, diabetes and ageing was seen.

Naturally, up to this point, the relationship was one of correlation and no causal mechanism had been established. However, researchers were very interested in finding out more about the capacity and activity of human BAT as a therapeutic means of treating the various metabolic consequences of obesity. The majority of the consequent studies focused on this BAT adaptive thermogenesis response by exposing volunteers to cold.

A 2011 study 36 exposed individuals to short but intense cold (e.g. immersing a limb in ice-cold water). Whilst they showed that this does indeed increase energy expenditure, it’s a method that fails completely to correspond with day-to-day experience and is impossible to sustain over time.

Additional research demonstrated that such extreme cold exposure was not necessary to stimulate sustained physiologic adaptive thermogenesis. It could be stimulated by even mild cold exposure as that controlled within normal (and bearable) climate-controlled buildings. This was shown in a 2010 crossover study 37 which looked at the effects of the adaptive thermogenesis response to minimal changes in environmental temperature. Healthy volunteers underwent two 12-hour periods in a whole room calorimeter (Metabolic Chamber) at 19 and 24 °c to monitor energy expenditure (EE). Results indicated that such minimal modulation of environmental temperature was sufficient to increase EE by around 6%. Might not seem much but, if projected over a 24 hour period, it would represent a drop of 100 kcal in an individual of between 70-80 kg.

Hormonal axes and organ-system response to mild cold exposure.

In addition to burning extra calories, exposure to mild cold (with the resulting increase in non-shivering thermogenesis) was shown to be sufficient to drive an adrenergic response 38 , which promotes lipolysis39 (with fatty acids being the preferred substrate in BAT depots) and increased postprandial glucose disposal. Additionally, the intervention generated an increase in cortisol 40  and a state of relative insulin resistance during fasting, which indicate an activation of the stress response. These, and other responses are shown in the adjacent table.

The researchers point out that, although the magnitude of this change may appear insignificant – only one fifth of the negative energy balance recommended to achieve sustained weight loss – it is relevant to note that, over a 1-year period (all things being equal), these differences would be equivalent to a 20-day fast and to a daily 30-min walk at a moderate pace.

A subsequent 2013 study 41 confirmed BAT contributes to energy expenditure (EE) in response to mild cold exposure – namely, 12-hour metabolic chamber exposure to either 19 or 24 ° C.

Two other 2013 studies showed, in the first case 42 , that a short-term, moderate (10 days acclimatisation with exposure at 17 ° C daily for 2 hours) cold exposure was sufficient to increase the quantity of BAT, and, in the second case 43 , that a longer period of time (6 weeks acclimatisation with exposure at 17 ° C daily for 2 hours) resulted in “significant fat mass reduction“- as shown in the following photos and chart:

BAT activation was shown to improve glucose homeostasis 44 and insulin sensitivity 45 in humans. Additional studies 46 47 looked at BAT and the hormone FGF-21 (fibroblast growth factor 21 production). FGF-21 is a critical metabolic regulator that governs glucose and lipid (fat) metabolism and plays an important role in the treatment of metabolic diseases, such as T2D (type 2 diabetes) and obesity. In T1D (type 1 diabetes), FGF-21 also reduces blood glucose levels and prevents diabetic complications.  It was demonstrated that BAT activation through cold exposure can up-regulate circulating FGF-21 in humans by 37%. FGF21 improves insulin sensitivity and glucose metabolism which may partially explain its longevity promoting benefits.

This offers hope for those with impaired insulin function who might benefit from BAT activation. And it’s not just those with clinically impaired insulin function, such as type 2 diabetics, who could benefit from this. Over time, even mildly elevated blood glucose levels in otherwise healthy non-diabetic humans are associated with other physiological damage. This has been shown to result in higher levels of the damaging AGE’s (advanced glycation end products – found in animal products, processed and fried/barbecued/roasted fatty foods), as well as damage to the brain, eyes, tendons, endothelial cells and the cardiovascular system 48 49 50 .

In a longer 2014 study 51 over four consecutive months, environmental temperature was modulated overnight – 24 ° C (run-in period), (cold acclimatisation), 24 ° C (wash-out period), and 30 ° C (heat acclimatisation). After a month of exposure to mild cold (19 ° C ), BAT volume and activity almost doubled, but after a month of exposure to warm temperature (30 ° C), BAT activity was negligible. The researchers commented that: “Remarkably, the increase in BAT activity following the cold acclimatisation was accompanied by a significant increase in postprandial glucose disposal, but only during mild cold exposure.

One study 52 looked at levels of irisin (a relatively newly discovered hormone) as a result of both intense exercise and cold exposure. Irisin is nicknamed the “exercise hormone” since  it’s released during moderate aerobic endurance activity and is known to be an anti-obesity and anti-diabetes hormone that regulates fat tissue and blood sugar, improving insulin sensitivity, bone quality/quantity 53 54 , and building lean muscle mass. In essence, irisin is thought to help reduce obesity by converting white fat to brown fat 55 . Being that irisin is released by muscles during physical exercise 56 , if cold-exposure also releases irisin, then perhaps the metabolic benefits of such exposure would be similar to those when irisin is released through exercise. And, indeed, this study demonstrated that this appears to be the case.

And irisin has other interesting effects. A study 57 on the reasons why healthy centenarians are healthy noted that they tend to have increased serum irisin levels, whilst irisin levels were significantly lower in younger patients with myocardial infarction 58 . So, although somewhat an aside to the main thrust of this blog, such findings are likely to prompt further research into the role of irisin in vascular disorders and life span extension.

Another hormone, adiponectin 59 , has associations with both BAT activation and centenarians. It’s been shown 60 that when BAT is activated through cold exposure, adiponectin levels increase within just two hours, resulting in a 70% increase in circulating adiponectin in adult men. Interestingly, both male and female centenarians (as well as their offspring) have been found 61  both to have genetics which boost adiponectin and to have generally higher circulating levels of adiponectin. This suggests a further link between BAT activation and longevity – this time because of the increased production of adiponectin. Furthermore, these high concentrations of plasma adiponectin in centenarians were associated 62 with other favourable metabolic factors as well as with lower levels of C-reactive protein 63  and E-selectin64 . It was mentioned earlier that BAT activation results in the production of FGF-21 – a hormone that improves insulin sensitivity and glucose metabolism. The latter benefits may explain why this hormone has been shown 46  to play a role in promoting longevity in humans.

In relation to fat and irisin, it was shown 65 that applying irisin to human preadipocytes (cells that can be transformed into different fat cells through the process of adipogenesis) , ordinary white adipocytes could be changed into beige adipocytes. This helps confirm the role of irisin as a myokine66 that can expand beige adipocyte mass, increasing the non-shivering thermogenesis capacity and, thereby, promoting a shift from inefficient and non-sustainable shivering thermogenesis to more efficient and sustainable non-shivering thermogenesis. In the following diagram, FGF-21 (fibroblast growth factor 21) promotes BAT’s activity of cold-induced non-shivering thermogenesis in humans.

Model of interplay between shivering and non-shivering thermogenesis. Exposure to cold promotes shivering in non-acclimated individuals, with the release of irisin. This response is unsustainable and costly from an energy-conservation perspective. Irisin promotes the expansion and differentiation of beige adipocytes, which increase resilience to cold enhancing non-shivering thermogenesis and delays the onset of shivering.

All the above studies indicate both that human BAT is extremely plastic, and that activation via cold exposure is necessary to generate a significant metabolic response.

Final thoughts

So, merely reducing the environmental temperature in your home could help to lose some body weight (represented by an additional energy expenditure of around 100 kcal) without actually undergoing exercise or changing one’s dietary habits. However, the amount of body fat you could lose through undergoing even colder and, consequently, more uncomfortable temperatures is something that I can’t imagine many people wanting to opt for as a weight-loss method.

Of course, integrating a bit of low temperature “therapy” might reduce one’s heating bills. And, of course, there is another weight-loss method associated with temperature modulation – namely, sweating your socks off in a sauna, albeit really just water that you’ll lose, and you’ll put the weight back on pretty soon afterwards when you rehydrate.

However, there is another simple non-exercise/non-dieting weight-loss method which is similar in effect to turning down the thermostat – namely, something called a standing desk. A standing desk is simply a matter of raising the height of one’s table (and hence the computer , book or paperwork thereon) and standing instead of sitting. Interestingly, this method has been shown 67 to increase calories burnt (in this case in young schoolchildren):

Another study 68 found that standing burned an extra 0.15 calories per minute, on average, compared with sitting. Men burned an extra 0.2 calories per minute while standing, which was twice as much as women, who burned an extra 0.1 calories. This was because men they typically have more muscle mass than women. This would mean that a person weighing around 63 kg (140 pounds/10 stones), replacing sitting with standing for six hours a day would burn an extra 54 calories per day.

Naturally, pharmaceutical companies may well try to come up with a “magic pill” that will stimulate BAT activity without the need for subjecting oneself to cold temperatures – maybe an injection or pill to stimulate BAT activity without having to ensure cold temperatures; but experience teaches us that most of these pharmaceutical wonder cures have unpleasant side effects and rarely prove as effective as their manufacturers initially claim.

So, whether of itself, or even when combined with another simple non-exercise/non-dietary change weight-loss method, it would seem that the benefits are interesting, though not comparable with the weight-loss benefits of a combination of exercise and eating a low-fat plant-based diet.

References & Notes

  1. Adipocytes are cells specialised in fat storage and are found in connective tissue. []
  2. Hany TF, Gharehpapagh E, Kamel EM, Buck A, Himms-Hagen J, von Schulthess GK (2002) Brown adipose tissue: a factor to consider in symmetrical tracer uptake in the neck and upper chest region. Eur J Nucl Med Mol Imaging 29: 1393– 1398. []
  3. Agrawal A, Nair N, Baghel NS (2009) A novel approach for reduction of brown fat uptake on FDG PET. Br J Radiol 82: 626– 631. []
  4. PET stands for positron-emission tomography (PET) and is a nuclear medicine functional imaging technique that is used to observe metabolic processes in the body as an aid to the diagnosis of disease. FDG stands for fludeoxyglucose, an analogue of glucose – the biologically active tracer molecule chosen for this type of scan. []
  5. Yeung HW, Grewal RK, Gonen M, Schöder H, Larson SM (2003). “Patterns of (18)F-FDG uptake in adipose tissue and muscle: a potential source of false-positives for PET”. J Nucl Med. 44 (11): 1789–96. []
  6. Huttunen P, Hirvonen J, Kinnula V (1981) The occurrence of brown adipose tissue in outdoor workers. Eur J Appl Physiol Occup Physiol 46: 339– 345. []
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  58. Myocardial infarction is commonly known as a heart attack, and occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw. []
  59. Adiponectin is a protein hormone that is produced by fat cells. Its physiological effects include the reduction of inflammation and atherogenesis (the formation of fatty deposits in the arteries) and enhancement of the response of cells to insulin. []
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  63. High C-reactive protein (CRP) levels in your blood indicate inflammation in your body, possibly indicating an infection or other condition. []
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Vegan Pie Comes Top in British Pie Awards 2019

Oh the scandal! The outrage! Grass-eaters winning a competition that should be dominated by pies filled with traditional steak and kidney, bacon and egg, pork and venison? And, to top it all, taking place in the hallowed heart of pork pie heaven, Melton Mowbray – the home of the classic pork pie.

For the sensitive souls (and taste buds) of the noble omnivore, this egregious affront to human taste and dignity comes far too soon on the back of Greggs’ launch of their ridiculously successful vegan sausage roll 1 . So successful, indeed, that it’s been credited as the cause of the 7% rise in the company’s share value 2 .

The vegan “pie” was produced by a company called Jon Thorner’s of Somerset 3 . As if it wouldn’t be so bad winning just one prize, they ended up winning a total of three awards at the recent 2019 British Pie Awards 4  for their Curried Sweet Potato & Butternut Squash, namely: “Best in Class”, “Best Producer” and “Supreme Pie Champion 2019”, beating 886 other competitors 5 at the contest in Melton Mowbray, Leicestershire 6 .

The leading chef, Richard Corrigan 7 , has blasted this butternut squash thing “a disgrace”. And, surely, the opinion of this Michelin-starred chef should be honoured and respected when he calls it a “pie in the sky”. All sane gastronomes will be relieved when he promises to make his “pig’s feet and black pudding and Swede pie” the next prize winner. 8

That’ll show those lily-livered lentil lovers!

While being interviewed by the Telegraph 9 , this bastion of butchery, who has proved his credentials as an arbiter of taste by having cooked for the Queen not once, but twice – showed how deeply affected he was by this culinary onslaught by uttering: “Please, please I’m going to cry.”

And, in support of the moderate and fair majority of people, he reminded us all of what proper food should be: “Pies are supposed to be filled with the most delicious morsels of steak and liver and kidney, with the jelly and little pieces of fat in the middle delicately dripping onto your tongue.

As though we’ve not had enough of populist nonsense – what with Brexiteers bandying around such outdated words like “democracy” and “national pride”. But to now have this travesty inflicted upon our already bowed and bruised heads by…one can hardly bear to say the word…v e g a n s.

As Chef Corrigan explains: “The oldest culinary art form left in the world and the vegans have taken it away. It’s a disgrace…The millennials have taken over…We should all just retire now.”

Matthew O’Callaghan, chairman of the 2019 British Pie Awards, appears to have slipped from the comforting embrace of omnivore common sense when he claims: “This year’s Supreme Champion was outstanding and well deserving of the accolade. From its very appearance on the judging tray you knew it was going to do well and it didn’t disappoint when it was opened and tasted. This pie isn’t just for vegans, it’s a pie for everybody. With this award we can truly say that veganism is now entering the mainstream of British food.” 5

The scale of the challenge ahead from marauding lettuce-lovers should not daunt the still-virtuous veganphobic nation of true meat-eaters.

Even as the faceless hordes of herbivores lay siege to the once great nation and its noble gastronomic traditions, I am reminded of John of Gaunt’s spirit-raising words of encouragement, as he lay on his death bed in Act One of Shakespeare’s Richard II:

“This royal throne of kings, this scepter’d isle,
This earth of majesty, this seat of Mars,
This other Eden, demi-paradise,
This fortress built by Nature for herself
Against infection and the hand of war,
This happy breed of men, this little world,
This precious stone set in the silver sea,
Which serves it in the office of a wall,
Or as a moat defensive to a house,
Against the envy of less happier lands,
This blessed plot, this earth, this realm, this England,
This nurse, this teeming womb of royal kings,
Fear’d by their breed and famous by their birth,
Renowned for their deeds as far from home,
For Christian service and true chivalry,
As is the sepulchre in stubborn Jewry,
Of the world’s ransom, blessed Mary’s Son,
This land of such dear souls, this dear dear land,
Dear for her reputation through the world,
Is now leased out, I die pronouncing it,
Like to a tenement or pelting farm:
England, bound in with the triumphant sea
Whose rocky shore beats back the envious siege
Of watery Neptune, is now bound in with shame,
With inky blots and rotten parchment bonds:
That England, that was wont to conquer others,
Hath made a shameful conquest of itself.
Ah, would the scandal vanish with my life,
How happy then were my ensuing death!”

He may as well have been making this speech now, just as the lights are being extinguished in the finest meat and two veg eateries across our nation…

Final thought

Now, I’m not claiming that the likes of Thorner’s vegan pie or Greggs’ vegan sausage roll are either ideal foods for optimal human health or what I would recommend as part of a WFPB diet – except maybe the very occasional “treat” to remind ourselves of what too much added salt and oil taste like. I mean, the name of my Greggs’ blog (“Greggs’ Vegan Sausage Rolls – Why Veganism Can Fail“) was not chosen for no reason!

However, the amount of venom spewed out by newspaper readers is somewhat over-the-top by anyone’s standards.

Such as some of those following the Telegraph article  9 :

  • What’s the problem? They are made out of Vegans, aren’t they?”
  • “I can’t eat grass; animals can. I can eat animals.”
  • “Sorry, vegans. I only eat fatty pork pies, or pies with succulent chunks of cow floating in ale and gravy.”
  • You can keep your veggie rubbish.”
  • “I’m with Mr Corrigan: if it’s “vegan” you can’t call it a pie. That would be an insult to the centuries of gloriously rich, meaty, aromatic, mouth-watering pies that have gone before. A non-meat snack for trendy neurotics, perhaps?”
  • Meat is good and the majority of people will not succumb to this utter BS.”
  • Also why salad lovers liberally apply dressing: because chomping on grass is not for humans it’s for ruminants. Cows eat the grass, we eat the cows, that’s the way the food chain works.”
  • You do know you’re made of meat right? And when your vegan body starts to starve you start to digest it to survive. That will be the least of your problems.”

And if you think that trying to educate people about veganism is a bit of a challenge, try espousing the virtues of a non-SOS WFPB diet. You’d lose count of the toys thrown out of prams.


  1. Greggs’ Vegan Sausage Rolls – Why Veganism Can Fail []
  2. The Guardian: Success of vegan sausage roll gives Greggs surge in sales []
  3. Jon Thorner’s of Somerset []
  4. British Pie Awards – 2019 []
  5. LeicestershireLive: Vegan pie named ‘supreme champion’ at British Pie Awards – for the first time ever [] []
  6. Location of Melton Mowbray, Leicestershire. []
  7. Wikipedia: Richard Corrigan. []
  8. Richard Corrigan: Facebook. []
  9. Telegraph. 8 March 2019: British Pie Awards 2019: Vegan pie is crowned Supreme Champion . [] []

Vitamin B12 Status in Spanish Veggies & Vegans

A previous blog 1 looked at a pre-published study on vitamin B12 status in Spanish vegetarians and vegans. Because there are very few reports on plant-based dietary patterns in Spain, this blog will look at the same study 2 in more detail, now that it has been published in its final form. While looking at B12 status amongst lacto-ovo vegetarians (LOV) and vegans (VN), it became clear that establishing true levels of this vitamin is a much more complex matter than most people realise. And, since side-effects of B12 deficiency are so nasty, this might be a blog worth reading – especially if you’re a plant-eater.

Thus, before looking at this study, it’s worth going into a bit more detail about vitamin B12.

Why is B12 status so important?

In normal healthy bodies, vitamin B12 (cobalamin) is readily absorbed in the distal ileum (the last part of the small intestine). However, in order for it to be absorbed, it must combine with a vital substance called intrinsic factor, which is a glycoprotein secreted by parietal cells of the gastric mucosa within the stomach. Without intrinsic factor, vitamin B12 will simply pass through the body and get excreted in stools.

Both vitamin B12 and vitamin B9 (folate) are necessary for the formation and maturation of red blood cells (erythrocytes) and the synthesis of DNA – the genetic material of cells. Vitamin B12 is also necessary for normal nerve function.

Since B12 is so essential for the formation of mature blood cells, any deficiency of this vitamin can result in anaemia, causing the body’s cells to receive insufficient oxygen from the haemoglobin within the red blood cells.

There are actually two forms of anaemia related to B12 deficiency and both are referred to as macrocytic anaemias 3 which can be either megaloblastic or pernicious anaemia:

Megaloblastic anaemia

This is characterised by abnormally large red blood cells (macrocytes) and abnormal white blood cells. It may not develop until 3-5 years after the deficiency starts. This is because around 3-5 years worth of B12 can be stored in the liver – so long as you’re an adult who has already been able to store sufficient quantities. No other B vitamin (or vitamin C) can be stored in the body like this, since they are all water-soluble (including B12) and are generally flushed out of the body if there is excess within the diet. On the other hand, the fat-based vitamins (A, E, D and K) can be stored in fat tissues as well as the liver. This means that daily intakes of the water-based vitamins (vitamins C, B1, B2, B3, B5, B6, B7, B9 and B12) is really important for maintenance of optimal health.

Megaloblastic anaemia is where insufficient B12 (or folate) is available to allow the normal DNA synthesis of red blood cells. It can be due to a number of causes, including:

  • insufficient B12 in the diet
  • overgrowth of bacteria in part of the small intestine
  • impaired absorption (malabsorption disorders such as coeliac disease or certain pancreatic disorders)
  • inflammatory bowel disease (IBD)
  • fish tapeworm infection
  • AIDS
  • surgery that removes the part of the small intestine where vitamin B12 is absorbed
  • drugs such as antacids and metformin (used to treat diabetes)
  • repeated exposure to nitrous oxide (laughing gas)
  • lack of intrinsic factor (see pernicious anaemia below)
  • decreased stomach acidity (common among older people)

As we age, our ability to absorb B12 decreases. This happens irrespective of dietary habits, but obviously there’s a bigger threat of deficiency (in all ages) for those who don’t eat animal products- the major source of B12. Bacteria in the soil and elsewhere produce B12. Animals don’t actually produce it themselves. If we still drank from pure streams and ate food we picked up from untreated soils, we’d get sufficient B12. However, with chlorinated water, pesticide-treated soils, and shrink-wrapped food, we either have to eat animal products or take supplements to ensure we get enough B12. There are plants that contain some of the vitamin (see below), but they are generally considered insufficient on their own to maintain healthy B12 levels.

Pernicious anaemia

Pernicious anaemia is a form of megaloblastic anemia where intrinsic factor is lacking. There may well be plenty of B12 in the diet, but if intrinsic factor is not present or, for some other reason, is not able to play its role in the the absorption of vitamin B12 from the small intestine into the bloodstream, then the B12 passes through and out of the body. This may be due to a number of reasons. For instance, abnormal antibodies, produced by an overactive immune system, may attack and destroy the parietal cells in the stomach that produce intrinsic factor, resulting in an autoimmune reaction called autoimmune metaplastic atrophic gastritis. Alternatively, intrinsic factor may be lacking because the part of the stomach where intrinsic factor is produced has been surgically removed.

Symptoms of B12 deficiency

Anaemia caused by vitamin B12 deficiency develops gradually. This allows the body to adapt to some extent, but this can mean that symptoms are mild while the anaemia is actually very severe.

Mild anemia symptoms can include:

  • paleness
  • weakness
  • fatigue

More serious anaemia symptoms can include:

  • shortness of breath
  • dizziness
  • rapid heart rate
  • spleen and liver enlargement

Pernicious anaemia in younger adults (due to lack of intrinsic factor) is more likely to result in the development of stomach and other gastrointestinal cancers.

B12 deficiency and nerve damage

Because B12 plays a significant role in the synthesis and maintenance of myelin4 , prolonged deficiency can result in damage to the central (CNS) and peripheral (PNS) nervous systems. In relation to CNS damage, white matter of the spinal cord and brain can suffer, resulting in such conditions as subacute combined degeneration (SCD) 5 and optic nerve atrophy. PNS issues are commonly manifested as nerve damage to the legs and arms, with the legs usually being affected earlier and more often than the arms. Symptoms include:

  • tingling in the feet and hands
  • loss of sensation in the legs, feet, and hands
  • weakness in arms and legs
  • loss of position sense – that is, people can’t tell so well where their arms and legs are and fail to feel vibrations
  • mild to moderate muscle weakness
  • loss of normal reflexes
  • difficulty in walking

In addition to the above neurological effects, some people can also become confused, irritable, and mildly depressed.

Advanced vitamin B12 deficiency may lead to delirium, paranoia and impaired mental function, including dementia.

Diagnosis of B12 deficiency

Diagnosis is via:

  • blood tests
  • the Schilling test (often in younger patients)
  • endoscopy
Blood tests

Routine serum blood tests can often show a suspected B12 deficiency if large red blood cells are detected. Since folate (vitamin B9) is also responsible for red blood cell synthesis, a possible B9 deficiency would normally also be investigated.

B12 deficiency can also be suspected if people complain of the typical symptoms associated with nerve damage, such as tingling or loss of sensation. If the deficiency is suspected, the level of vitamin B12 in the blood is measured.

Additionally, serum gastrin 6  levels or autoantibodies 7  to intrinsic factor may be measured.

Schilling test

The Schilling test involves the patient being given two doses of B12. The first is ‘labelled’ with a small amount of a radioactive substance and is then taken by mouth. The second is an injection one hour later of a larger amount of B12 that is not radioactively labelled, which is used in order to prevent any of the labelled B12 from binding to B12-depleted tissues.

After the injection is given, the amount of labelled B12 (that which had been taken orally) is measured by testing the urine to determine whether the body absorbed a normal (digested, rather than injected) amount of the vitamin.

If this normal amount has not been absorbed (revealed by a high amount being found in the urine), then the deficiency is confirmed. The same test is then repeated. This time, people are given intrinsic factor with the B12 taken by mouth. If intrinsic factor enables the body to absorb more of the vitamin, then it’s confirmed that the deficiency is caused by a lack of intrinsic factor, and the diagnosis of pernicious anemia can be made. If the B12 is still not absorbed, further tests are undertaken to check for potential problems with pancreatic enzymes or bacterial abnormalities.

More detail on this test can be found here 8 .


Endoscopy is the use of a flexible viewing tube to directly examine internal structures. It may be done to check for destruction of the parietal stomach cells that produce intrinsic factor.

If vitamin B12 deficiency is confirmed in an older person, it’s unlikely that either Schilling or endoscopy will be used. This is because the cause is likely to be the usual age-related reduction in stomach acidity, and is usually not serious. However, in a younger person, other tests, including other blood tests, Schilling test and endoscopy are likely to be used in order to establish intrinsic factor status.

Folate, B12 deficiency & plant-based diets

It’s important to note that high folate (vitamin B9) levels can give a false negative for B12 deficiency. That is, high levels of folate in the blood sample can make it look like there’s no B12 deficiency. This is because the constant supply of folate allows the red blood cells to appear normal in size, while the other serious neurological damage of B12 deficiency can go unnoticed, in spite of the person having regular blood tests for B12 deficiency.

Of course, those people most likely to have a B12 deficiency while having high dietary folate intake are those eating a plant-based diet – given that there’s so much folate in plant foods. This is why B12 supplementation is so important.

Treatments for B12 deficiency

For less advanced deficiency, B12 supplements generally do the trick; however, if people already have nerve damage, or they have pernicious anaemia (for instance, caused by having had the part of the stomach removed which produced intrinsic factor), then the B12 is normally given by injections into a muscle for defined periods so long as the disorder is uncorrected.

Since the B12 in supplements is easier to absorb than that in meat, older people with deficiency can benefit from taking B12 supplements.

In most people with mild to moderate anaemia, there is a normalisation in around 6 weeks of treatment with high doses of B12 supplements. However, in severe cases due to nerve damage or loss of ability to produce intrinsic factor, the treatment by B12 injection could last for the rest of their lives.

Unfortunately, in those with dementia resulting from B12 deficiency (mostly older people), mental function would not be expected to improve after treatment.

How much B12 should I supplement?

I covered this subject in some detail in a previous blog 9 , which I suggest you take a look at if you are unsure about how often and how much B12 you should be supplementing.

Non-animal foods containing vitamin B12

Several mushroom species contain some B12, including:

  • shiitake (Lentinula edodes)
  • black trumpet (Craterellus cornucopioides), and
  • golden chanterelle (Cantharellus cibarius)

Certain algae and cyanobacteria 10 such as:

  • chlorella 11 , and
  • spirulina (Arthrospira platensis12

The above are some of the foods normally used to produce B12 supplements for veggies and vegans.

Animal foods containing B12

Animal sources highest in vitamin B12 include meats (especially beef, pork, liver, and other organ meats), eggs, fortified cereals, milk, clams, oysters, salmon, and tuna.

It’s been reported that B12 deficiency exists much more widely in omnivore populations than one might imagine, since modern animal rearing practices are causing a reduction in the levels of B12 in meat. This can be seen particularly clearly, for instance, in the need to given cobalt supplements to cattle and sheep because of the reduced levels of cobalt in modern cultivated soils (B12 is called cobalamin because it contains a cobalt atom) 13 .

The Spanish study 2

The 49 lacto-ovo vegetarians and 54 vegans in the study filled out a Food Frequency Questionnaire (FFQ), and were tested to establish the following classical and functional markers (explanation of all terms in green can be seen by holding the cursor over the adjacent footnote number):

  • serum B12 14
  • erythrocyte folate (vitamin B9) 15
  • homocysteine (Hcy) 16 / hyperhomocysteinaemia (HHcy) 17  
  • methylmalonic acid (MMA) 18
  • mean corpuscular haemoglobin (MCH) 19
  • mean corpuscular erythrocyte volume (MCV) 20

In broad terms, two parts of this study are of particular interest: firstly, the difficulties involved in accurately diagnosing B12 deficiency (and the suggested additional tests by which this can be more accurately diagnosed) and, secondly, to see if there was any pattern of B12 deficiency between the two groups – lacto-ovo-vegetarian (LOV) and vegan (VN).

1. Difficulties in diagnosing B12 deficiency

In order to understand the potential difficulties involved in diagnosing B12 deficiency, it’s useful to understand the vital processes B12 undergoes within the body, and this will involve knowing about two biological cycles: the methionine cycle and the folate cycle, both of which are essential for DNA and RNA synthesis, the production of red blood cells (erythropoiesis) and the production of neurotransmitters. 21 22

Vitamin B12 acts as a cofactor 23 of the enzymes methionine synthase 24 , which acts in the conversion of homocysteine (Hcy) to methionine, and methylmalonyl-CoA mutase 25 , that produces succinyl-CoA from methylmalonyl-CoA, the active form of methylmalonic acid (MMA)18 .

The above reactions are involved in the methionine cycle 26 and the folate cycle 27 , both essential for DNA and RNA synthesis, erythropoiesis and the production of neurotransmitters.

The folate cycle is so important to the methionine cycle (also called the methylation cycle) that it’s often included in descriptions and diagrams of the methionine cycle. The following diagram should give you an idea of how interlinked and complex these cycles are.

Problems with Serum B12 tests

As mentioned above, testing levels of serum B12 is probably the most widely used means of assessing deficiency. However, a major problem is that it can appear perfectly normal whilst, at the same time. functional deficiency still lurks unseen beneath the surface. The long latency period of B12 deficiency showing up in the blood serum can regularly produce both false positives and false negatives – that is, appearing to have a deficiency but not having one, or not appearing to have a deficiency but actually having one. 28

Folate (vitamin B9) & B12

Since it’s known both that high levels of folate can mask B12 deficiency and that low levels of folate can account for hyperhomocysteinaemia (HHcy)17 , it follows that testing for folate levels would be rather useful. By establishing that folate levels are high (as they are likely to be in most plant-eaters – unless, of course, they’re living on a diet of doughnuts and chips!) , it would be possible to quickly discard folate deficiency as being responsible for HHcy or the presence of megaloblastic anaemia. 29

Homocysteine & B12

Testing for homocysteine (Hcy) levels – a more specific marker of functional vitamin B12 deficiency – would be a useful additional test. This is because Hcy levels rise in the presence of cellular B12 deficiency. So, is that sorted, then? Well, not quite. Another problem arises – namely, that Hcy levels can also be raised with deficiencies of vitamins B9 (folate) or B6 (pyridoxine) as well as by diets rich in methionine 30 . So back to the drawing board.

Methylmalonic acid (MMA) & B12

So, what about testing for MMA levels? This represents probably the most specific marker for vitamin B12 deficiency, since it’s independent of folate and vitamin B6 status. MMA levels increase when there’s a B12 deficiency, and this happens even before there are any obvious clinical symptoms of the deficiency.

The more the merrier

So, the researchers in this study suggest that when testing for B12 deficiency, relying on just one single standard marker of deficiency is to be avoided. Instead, several markers should be used – levels of serum B12/B9, Hcy and MMA 31 .

2. B12 status of Spanish lacto-ovo-vegetarians & vegans

Finally, we come to the findings of this study:

  • the overall prevalence of clinical vitamin B12 deficiency was very low in the individuals tested
  • when serum B12 levels alone were tested, there was no indication of B12 deficiency in either diet group

Various B12 markers

However, when MMA was measured, some subclinical deficiencies were detected, particularly in the non-users of vitamin B12 supplements, with no significant differences between VN and LOV. With elevated MMA being detected in more than 10 % of the study subjects, it’s clear that using this marker to detect subclinical deficiencies is a pretty good idea.

  • although macrocytosis (enlarged red blood cells) was observed in several participants, no clear relationship to any biomarkers of vitamin B12 deficiency could be found
  • HHcy was found in more than 30 % of the subjects

They recommend that both MMA and Hcy (together with serum B12) should be used since each of these biomarkers gives information about the actions of B12 in different metabolic pathways. For instance, the metabolic reactions leading to the production of MMA and Hcy require different cobalamin forms:

  • methylcobalamin acts in the Hcy pathway
  • adenosylcobalamin acts in the formation of succinyl-CoA

The latter occur in different cell compartments:

  • the methionine and folate cycles occur in the cell’s cytoplasm 32
  • the synthesis of succinyl-CoA (SCS) 33  occurs in the mitochondria34

When B12 status was assessed with serum vitamin B12, MMA and Hcy simultaneously, the proportion of subjects with values out of range of at least one of the biomarkers was remarkably higher than the proportion detected by using only serum B12.

Most of the hyperhomocysteinaemic individuals presented mild HHcy (16–30 µmol/l) while only three volunteers had moderate HHcy (31–100 µmol/l).

Hcy variation in veggies from different European countries

Interestingly, this study comments on the fact that there’s great variability in the B12 values obtained in vegetarians from different European countries:

  • German vegetarians had lower Hcy levels 35
  • Slovak and Austrian vegetarians had higher Hcy levels 36

In the current study, Hcy was higher in LOV than in VN, which contrasted with other studies 37 .

High folate levels

Erythrocyte folate levels were high in all participants, with more than 50 % surpassing the suggested 38 cut-off for high erythrocyte folate (1360 nmol/l). This is in line with other research 39 that found higher folate intakes in plant-eaters than in omnivores.

Methionine & Hcy/HHcy

With folate repletion and under similar B12 levels, it was observed that LOV had higher levels of both Hcy and HHcy than VN. The researchers said this might be due to the fact that LOV consume more protein and, thus, more methionine, being that both dairy and egg are higher in methionine than plant foods. By increasing blood levels of Hcy, high methionine levels are linked to increased risk of heart disease, tumour growth, brain damage and even death.

The importance of supplementation

Various studies 37 have reported lower B12 levels in vegans, but this was not observed in the present study. The reason for this is thought to be that the members of both Spanish groups had a high and extended use of cobalamin (B12) supplements, with B12 supplement users exhibiting higher serum B12 and erythrocyte folate levels (as well as lower MMA and Hcy) than non-users. This underlines the importance of supplementation for vegans and lacto-ovo vegetarians.

These results are, of course, consistent with previous studies that recommend intake of B12 in supplement form. The reason generally given – which seems perfectly fair – is that it’s difficult for plant-eaters to achieve consistent and sufficient B12 levels without taking B12 supplements. The intake of fortified food items is not enough, of itself, to provide the required doses of the vitamin.40 41

Supplementation, diet or socioeconomic variation?

In recent studies on vegetarian Indians 42 43 , a prevalence of B12 deficiency was found in around 70 % of those tested, with more than 50 % of the subjects also presenting HHcy.

An explanation for this variation between results from Spain and India may be explained by differences in both diet composition and socioeconomic status. 44 

However, even in studies of B12 status in European countries (where one would expect vegetarians to have similar socioeconomic status and diet composition as found in Spain), similar differences (that is, less B12 deficiency in Spanish vegetarians) was seen in Germany, the Netherlands and the UK. 45

Thus, the researchers maintain that the sufficient B12 status observed in both Spanish groups (LOV and VN) can be mainly accounted for by the extended use of cobalamin supplements in the Spanish participants compared with the lower amount of such supplementation reported in other European studies.

Spanish plant milks are not fortified

Having spent a significant time at our mountain retreat in Spain, it has always interested me that the Spanish do not fortify their plant milks – unlike the UK and elsewhere in Europe. This is a very good reason why any veggie living (or spending extended periods) in Spain should not rely on plant milks for their B12. Indeed, the current study emphasises that such milks had no influence on the analysed biomarkers in this research, being that these milks are not B12-fortified.

Final thoughts

Two limitations of this study were, firstly, that they didn’t add an additional omnivore group for comparison, since this would have shown whether and by how much these groups (LOV and VN) differed from the general meat-eating Spanish population and, secondly, this was a small sample (103 individuals) from which to generalise to the whole Spanish LOV and VN population – of which veggies are thought 46 to comprise around 1.5%.

What would have been interesting, in addition, would have been to include a WFPB dietary group. Naturally, this is something that would prove very difficult in almost any country (perhaps excluding certain ‘enlightened’ populations within the US), since the number of people eating a WFPB diet is still very low.

The report did not consider the influence of any potential genetic polymorphisms 47 that might be involved in the B12 and folate routes. Perhaps future B12 studies could look at this, as well as include a larger number of subjects and include both omnivores and those eating a WFPB diet.

In any case, the take-home message is that anyone eating a plant-based diet needs to take B12 supplementation. It’s a cheap and highly effective way of avoiding health conditions that would undo some of the wonderful work achieved by eating this way.

References & Notes

  1. B12 Supplements Are Efficient But Caution With Folic Acid []
  2. J Nutr Sci. 2019 Feb 26;8:e7. doi: 10.1017/jns.2019.2. eCollection 2019. Vitamin B12 and folate status in Spanish lacto-ovo vegetarians and vegans. Gallego-Narbón A, Zapatera B, Barrios L, Vaquero MP. [] []
  3. The term macrocytic is from Greek words meaning “large cell”. A macrocytic class of anaemia is an anaemia (defined as blood with an insufficient concentration of haemoglobin) in which the red blood cells (erythrocytes) are larger than their normal volume. []
  4. Myelin is an insulating layer, or sheath that forms around nerves, including those in the brain and spinal cord. It is made up of protein and fatty substances. This myelin sheath allows electrical impulses to transmit quickly and efficiently along the nerve cells. []
  5. Subacute combined degeneration (SCD) is characterised by symmetric dysesthesia, disturbance of position sense and spastic paraparesis or tetraparesis. []
  6. Gastrin is a hormone which stimulates secretion of gastric juice and is secreted into the bloodstream by the stomach wall in response to the presence of food. []
  7. An autoantibody is antibody produced by in response to a constituent of its own tissues. []
  8. Schilling Test Kamleshun Ramphul; Stephanie G. Mejias. Statpearls. []
  9. Vegan Society Veg-1: Does It Contain Enough B12? []
  10. Cyanobacteria are a division of microorganisms related to bacteria but which are capable of photosynthesis. They are prokaryotic and represent the earliest known form of life on the earth. []
  11. a genus of single-celled green algae belonging to the division Chlorophyta. []
  12. Spirulina is a biomass of cyanobacteria (blue-green algae) from the two species Arthrospira platensis and A. maxima. It can be consumed by humans and other animals. Arthrospira is cultivated worldwide and is used as a dietary supplement or whole food, being also used as a feed supplement in the aquaculture, aquarium, and poultry industries. []
  13. J Dairy Sci. 1979 Aug;62(8):1195-206. Trace element deficiencies and fertility in ruminants: a review. Hidiroglou M. []
  14. In blood, serum is the liquid part but without the clotting factors (mainly fibrinogens). The liquid part with the clotting factors is the plasma. Serum still includes all the other proteins not used in blood clotting, along with all the electrolytes, antibodies, antigens, hormones, and any exogenous substances. []
  15. Red blood cell (erythrocyte) folate concentrations respond slowly to changes in dietary folate intake since the erythrocytes, which have a 120-day lifespan, accumulate folate only during the production of new red blood cells (erythropoiesis). Red blood cell folate concentrations are useful as indicators of long-term folate status. []
  16. Homocysteine (an intermediate in the metabolism of the amino acids methionine and cysteine) is a common amino acid in your blood. You get it mostly from eating meat. High levels of it are linked to early development of heart disease. and is associated with low levels of vitamins B6, B12, and folate, as well as with renal disease. []
  17. Hyperhomocysteinaemia is a medical condition characterised by an abnormally high level of homocysteine in the blood, conventionally described as being above 15 µmol/L. Hyperhomocysteinaemia is typically managed with vitamin B6, vitamin B9 and vitamin B12 supplementation.  Hyperhomocysteinaemia promotes the formation of active oxygen species and the release of inflammatory mediators, and therefore it is considered a risk factor for cardiovascular disease (CVD). [] []
  18. Methylmalonic acid (MMA) is a substance produced in very small amounts and is necessary for human metabolism and energy production. The measurement of elevated amounts of methylmalonic acid in the blood or urine serves as a sensitive and early indicator of vitamin B12 deficiency. [] []
  19. Mean corpuscular haemoglobin is the average mass of haemoglobin per red blood cell in a sample of blood. High MCH levels are commonly a sign of the macrocytic anaemia seen in B12 or folate deficiency. []
  20. Mean corpuscular volume is a measure of the average volume of a red blood corpuscle. The measure is attained by multiplying a volume of blood by the proportion of blood that is cellular, and dividing that product by the number of erythrocytes in that volume. High MCV implies the red blood cells are larger than normal (i.e. macrocytic) and is a test of B12 and folate deficiency. []
  21. Krishnaswamy K & Madhavan Nair K (2001) Importance of folate in human nutrition. Br J Nutr 85, Suppl. 2, S115–S124. []
  22. Kapoor A, Baig M, Tunio SA, et al. (2017) Neuropsychiatric and neurological problems among vitamin B12 deficient young vegetarians. Neurosciences (Riyadh) 22, 228–232. []
  23. A cofactor is a non-protein chemical compound or metallic ion that is required for an enzyme’s activity. Cofactors can be considered “helper molecules” that assist in biochemical transformations. []
  24. Methionine is an essential amino acid that has to be derived from our diet. Methionine synthase is responsible for the regeneration of methionine from homocysteine. []
  25. Methylmalonyl-CoA mutase (MCM) is a protein that in humans is encoded by the MUT gene. This vitamin B12-dependent enzyme catalyses the isomerisation of methylmalonyl-CoA to succinyl-CoA in humans. []
  26. In the methionine cycle, methionine (a sulphur-containing amino acid which enters the body through dietary proteins) is used in forming proteins in the body. In the methionine cycle, methionine acts as the precursor of the sulphur-containing amino acids homocysteine, cysteine, and taurine. Taurine is one of the few amino acids not used in protein synthesis, and is thus usually referred to as a “nonessential” amino acid, or more generously as a “conditionally essential” amino acid. []
  27. Within the folate cycle, folate coenzymes are responsible for the one-carbon unit transfer in intermediary metabolism and are required for several reactions in key metabolic processes, for example of purine, pyrimidine and methionine synthesis, and glycine and serine metabolism. []
  28. Klee GG (2000) Cobalamin and folate evaluation: measurement of methylmalonic acid and homocysteine vs vitamin B12 and folate. Clin Chem 46, 1277–1283. []
  29. Krajcovicova-Kudlackova M, Blazicek P, Kopcova J, et al. (2000) Homocysteine levels in vegetarians versus omnivores. Ann Nutr Metab 44, 135–138. []
  30. Kumar A, Palfrey HA, Pathak R, et al. (2017) The metabolism and significance of homocysteine in nutrition and health. Nutr Metab (Lond) 14, 78. []
  31. Yetley EA, Pfeiffer CM, Phinney KW, et al. (2011) Biomarkers of vitamin B12 status in NHANES: a roundtable summary. Am J Clin Nutr 94, 313S–321S. []
  32. Cytoplasm is a thick solution that fills each cell and is enclosed by the cell membrane. It’s mainly composed of water, salts, and proteins. All the organelles, such as the nucleus, endoplasmic reticulum, and mitochondria, are located in the cytoplasm within eukaryotic cells. Organelles are the organised or specialised structures within a living cell. Eukaryotic cells are cells that contain a nucleus and organelles, enclosed by a plasma membrane. Humans are composed of eukaryotic cells and are thus grouped into the biological domain Eukaryota. Eukaryotic cells are larger and more complex than prokaryotic cells, which are found in Archaea and Bacteria, the other two domains of life. []
  33. Succinyl-CoA or SCS facilitates the flux of molecules into other metabolic pathways by controlling the interconversion between succinyl CoA and succinate. This is important because succinyl CoA is an intermediate necessary for porphyrin, haem, and ketone body biosynthesis. It’s a necessary part of the energy-producing Krebs or citric acid cycle. []
  34. The mitochondria is an organelle found in large numbers in most cells, in which the biochemical processes of respiration and energy production occur – the “powerhouses” of energy production. []
  35. Waldmann A, Koschizke JW, Leitzmann C, et al. (2004) Homocysteine and cobalamin status in German vegans. Public Health Nutr 7, 467–472. []
  36. Majchrzak D, Singer I, Manner M, et al. (2006) B-vitamin status and concentrations of homocysteine in Austrian omnivores, vegetarians and vegans. Ann Nutr Metab 50, 485–491. []
  37. Elmadfa I & Singer I (2009) Vitamin B12 and homocysteine status among vegetarians: a global perspective. Am J Clin Nutr 89, 1693S–1698S. [] []
  38. Colapinto CK, O’Connor DL & Tremblay MS (2011) Folate status of the population in the Canadian Health Measures Survey. CMAJ 183, E100–E106. []
  39. Schüpbach R, Wegmüller R, Berguerand C, et al. (2017) Micronutrient status and intake in omnivores, vegetarians and vegans in Switzerland. Eur J Nutr 56, 283–293. []
  40. Gilsing AM, Crowe FL, Lloyd-Wright Z, et al. (2010) Serum concentrations of vitamin B12 and folate in British male omnivores, vegetarians and vegans: results from a cross-sectional analysis of the EPIC-Oxford cohort study. Eur J Clin Nutr 64, 933–939. []
  41. Pawlak R, Lester SE & Babatunde T (2014) The prevalence of cobalamin deficiency among vegetarians assessed by serum vitamin B12: a review of literature. Eur J Clin Nutr 68, 541–548. []
  42. Naik S, Mahalle N & Bhide V (2018) Identification of vitamin B12 deficiency in vegetarian Indians. Br J Nutr 119, 629–635. []
  43. Yajnik CS, Deshpande SS, Lubree HG, et al. (2006) Vitamin B12 deficiency and hyperhomocysteinemia in rural and urban Indians. J Assoc Physicians India 54, 775–782. []
  44. Menal-Puey S & Marques-Lopes I (2017) Development of a food guide for the vegetarians of Spain. J Acad Nutr Diet 117, 1509–1516. []
  45. Herrmann W, Schorr H, Obeid R, et al. (2003) Vitamin B12 status, particularly holotranscobalamin II and methylmalonic acid concentrations, and hyperhomocysteinemia in vegetarians. Am J Clin Nutr 78, 131–136. []
  46. AECOSAN (2011) National Survey of Dietary Intake (2009–2010). Results on Consumption Data. Madrid: Spanish Agency for Consumer Affairs, Food Safety and Nutrition Government of Spain. []
  47. Polymorphisms are the occurrence of different forms among the members of a population or colony, or in the life cycle of an individual organism. []

Flaxseeds / Linseeds – Lignan Heaven

There are a wide number of reasons why it’s a pretty good idea to add flaxseeds to your food shopping list, whether or not you’re eating a plant-based diet. These little seeds are a powerhouse of goodness. If, as a result of reading this blog, you’re encouraged to include them in your daily diet, then I’ll be pretty confident that, in a small way, I’ve helped you towards a longer and healthier life.

Is flaxseed the same as linseed?

If you enter either word in Wikipedia, you get exactly the same page. I guess this indicates that they are, to all intents and purposes, the same thing – members of the plant family Linaceae and the genus Linum. Whilst there are variations within the genus, the only major difference you’ll notice is that the seeds can be either brown or golden (yellow) in colour.

Although fibrous parts of the flax plant are used for various purposes (including making clothing), and you’ll know about the uses of linseed oil (including protecting cricket bats), we’ll just concentrate on the linseed/flaxseeds themselves, which will be herein referred to as flaxseeds for the sake of brevity. By the way, my advice is to avoid consuming any the the oil prepared from flaxseeds, for the same reason as all oils are to be avoided 1 . Instead, just stick to the seeds.

Why do flaxseeds need to be ground?

Unlike most seeds, the outer protective shell of each tiny flaxseed is so tough that eating them whole will mean they ‘cut out the middle man’ and end up, intact, in the toilet bowl. By grinding them, all the wonderful goodness is released. I go into this in a bit more detail later.

What’s the nutritional value of flaxseeds?

Most flaxseeds have an almost identical nutritional profile, with the same number of omega-3 fatty acids. This makes them a really important part of any plant-based diet. There is, however, one variant of yellow flax (solin, usually under the trade name “Linola”) which is very low in omega-3 fatty acids. Fibre, protein, and fat profiles are excellent.

You’ll see from the nutritional value chart 2 that there are also plenty of vitamins and minerals in flaxseeds. But the good news doesn’t end there. Of all the individual so-called ‘super foods’ that you could think of, flaxseeds will be right up there at the top. The lignan content is just one weapon in their disease-fighting armoury. Essential fatty acids (ALA and AA) and fibre content are also remarkably high. To give you an idea of just how amazing the bundle of compounds in flaxseeds really are, the following is a list of some of the health benefits that these amazing little fellas may offer:

  • lowering blood pressure 3 , hence:
    • helping to prevent heart attacks 4
    • helping to prevent strokes 5
  • fighting cancer
    • prostate cancer 6 7
    • breast cancer 8 9
  • lowering blood cholesterol levels 10
  • reducing blood triglyceride levels 11
  • reducing blood sugar levels/insulin resistance/diabetes risk 12 13 14
  • reducing inflammation 15 16
  • preventing/treating constipation 17
  • reducing body weight/BMI 18
  • preventing osteoporosis/bone loss 19 20
  • preventing arthritis 21
  • improving skin health/healing 22
  • reducing number of menstrual periods 23

Omega-3 & flaxseeds

As I’ve pointed out in previous blogs, flaxseeds 24 25  and chia seeds 26 (along with walnuts) are probably the best non-fish sources of omega-3’s for those eating a plant-based diet. The long-chain polyunsaturated fatty acid (LC-PUFA) ALA (alpha-linolenic acid) is an essential fatty acid which we need to get from our diet since the human body can’t synthesise it on its own. When sufficient ALA is provided in the diet, the body can use it to make the longer-chain PUFA’s, DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid), both of which are essential for our health. 27

The following diagrams illustrate the high levels of omega-3 oils in flaxseeds:

What are lignans?

From the Latin for “wood”  (lign-) plus the chemical suffix”-an”, lignans found in plants are a form of micronutrient called polyphenols 28 . In order for the plant lignans29 to be used by the human body, they have to be metabolised by our gut bacteria into the mammalian lignans called enterodiol and enterolactone (known as enterolignans – from the Greek énteron meaning intestine). So, plant lignans can be described as “lignan precursors” for our human versions.

Lignans are one of the major classes of phytoestrogens30 – oestrogen-like chemicals (found in foods like beans, seeds and grains) that also act as antioxidants. You’ll hear some comments on the internet that phytoestrogens are dangerous because they bind to and block important oestrogen receptors; however, this does not appear to be the case, since there are two different forms of oestrogen receptor, and phytoestrogens do not block those to which oestrogen normally attaches. Additionally, evidence exists 31 that they can help prevent cardiovascular diseases, diabetes and cancer of the breast, brain, colon, liver, ovaries and skin. They also appear to reduce LDL (“bad”) cholesterol and aid weight loss. While phytoestrogens found in plants do not decrease male fertility, the xenoestrogens 32, which, in terms of diet, are found mainly in fish, have been shown to drastically lower sperm count and cause early puberty.

Whilst the above long list 33 of health benefits offered by flaxseeds is, of course, also partly attributable to the other essential fatty acids, minerals, vitamins and phytochemicals they contain, the lignan content is especially powerful. Trying to decide exactly what each individual compound does is a really tough task, and perhaps not always necessary. After all, the compounds do not exist in isolation within plants and neither do they work in isolation within our bodies. Trying to pinpoint active compounds is something that pharmaceutical companies love to do, since they can then bottle them and sell them at high price, even though they often don’t work as they did when the compound was in its natural position within the complex of the original plant.

We’ve looked at the issue of wholism vs reductionism in a previous blog 34 . So, whether the cardiovascular protection afforded by flaxseeds is x% due to the omega-3, y% due to the fibre, and z% due to the lignans is, as far as I’m concerned, a secondary matter to what the whole seed is capable of doing with all three elements, plus the others we know about and the many we still haven’t even identified. And this doesn’t even touch on the vast array of interactions between these elements and the likelihood that there will be some variation between the physiology of individual humans – particularly in relation to the microbiome (gut, urinary, oral, etc) that our diets and lifestyles have provided us with.

In terms of lignans, why are flaxseeds so remarkable?

The type of lignans found in flaxseeds are not the only dietary lignans – others include sesamin 35 , matairesinol 36 , pinoresinol 37 and lariciresinol 38 . The main lignan in flaxseeds (as well as in sunflower, sesame, and pumpkin seeds) has the unpronounceable name “secoisolariciresinol diglucoside” or SDG for short. Regardless of the source of SDG, once it’s ingested, it’s “…converted in the colon into active mammalian lignans, enterodiol, and enterolactone, which have shown promise in reducing growth of cancerous tumors, especially hormone‐sensitive ones such as those of the breast, endometrium, and prostate. Known for their hydrogen‐donating antioxidant activity as well as their ability to complex divalent transition metal cations, lignans are propitious to human health.” 39 .  All well and good, but the remarkable thing about flaxseeds isn’t that the lignans they contain are not found in other seeds, rather it’s because of the incredibly high lignan content these little seeds have. Indeed, you’ll see from the following chart 40 that they contain around 100 times more lignans than almost every other food, with sesame seeds being the closest with 7 times less.

Add to this the fact that Dr Greger claims 41 there are no bad side effects to normal flaxseed consumption 42 – unless, of course, you’re one of the very few who has a flaxseed allergy 43 – and you have as near to a super food as you’re likely to get.

One study compared the results of flaxseeds and flaxseed oil: “SDG [the major type of lignan in flaxseeds] is a potent angiogenic and antiapoptotic agent that may have a role in cardio protection in ischemic heart disease. In conclusion, flaxseed, FLC, and SDG, but not flaxseed oil, suppress atherosclerosis, and FLC [flax lignan complex] and SDG slow progression of atherosclerosis but have no effect on regression. Flaxseed oil suppresses oxygen radical production by white blood cells, prolongs bleeding time, and in higher doses suppresses serum levels of inflammatory mediators and does not lower serum lipids.” 44

No lignans in flaxseed oil

It’s important to note that when you extract pure oil from flaxseeds, the important phytoestrogen lignans are removed 45 . This is another reason why it’s important to consume the whole seed and to generally keep away from extracted flaxseed oil – unless, of course, you want to grease your cricket bat! This rule applies to all extracted oils, of course, as mentioned above.

Flaxseed proteins

The following is a sample of research reviewed within one study 46  showing some of the varied health benefits from the proteins within flaxseeds:

Fatty acids in flaxseeds

The following chart (from the same study as above) indicates the levels of the major fatty acids within flaxseeds:

Historical & recent medicinal uses of flaxseeds

The following charts (from the same source as above) indicate some of the distant historical and more recent uses of flaxseeds (in the latter case, from flaxseed oil):

Microbiome & lignans

The nature of your gut bacteria (the intestinal microbiome) will affect how much of the lignan goodness is absorbed and utilised by your body. As one authority states: “It is likely that individual differences in the metabolism of lignans, possibly due to gut microbes, influence the biological activities and health effects of these compounds.” 47 As is the case with so much nutrient metabolism and absorption, having a healthy got microbiome is so important, and, as was shown in an earlier blog 48 a varied plant-based diet (as opposed to a meat- or processed food-based diet) provides by far the healthiest environment for intestinal bacteria.

How much ground flaxseed should we have each day?

Dr Greger can answer this for us. In response to one of the above-mentioned studies, entitled “Flaxseed: A Miraculous Defence Against Some Critical Maladies,” 3 , he states:

Miraculous”? Well, certainly super healthy, which is why a tablespoon of ground flaxseeds every day gets its own spot on the Daily Dozen checklist 49  I created to help inspire you to incorporate some of the healthiest foods into your daily routine.” 50

You can get your daily tablespoon of ground flaxseeds in so many ways: from mixing it in with your morning muesli to using it as a thickener in soups, stews, etc.

Dr Greger, flaxseeds & lignans

Talking about Dr G, you’d be able to get an idea of just how important a subject is by counting the number of videos he does on that subject. The following are just his most popular of videos which discuss the evidence for the lasting force of lignans and flaxseeds:

    • Which Are Better: Chia Seeds or Flax Seeds? 51
    • Flaxseeds for Hypertension 52
    • Can Flaxseeds Help Prevent Breast Cancer? 53
    • Flaxseeds for Breast Pain 54
    • Flaxseeds & Breast Cancer Survival: Clinical Evidence 55
    • Flaxseeds & Breast Cancer Survival: Epidemiological Evidence 56
    • Flaxseeds & Breast Cancer Prevention 57
    • Just the Flax, Ma’am? 58
    • Flaxseeds vs. Prostate Cancer 59
    • Flaxseeds vs. Diabetes 60
    • Was It the Flaxseeds, Fat Restriction, or Both? 61
    • Flaxseeds for Sensitive Skin 62
    • Flaxseeds vs. Chia Seeds 63
    • Which Are Better: Chia Seeds or Flaxseeds? 64

Final thoughts

It’s hard to believe that such a humble little seed can do so much good, but the evidence is there to support the claims – and the studies I’ve listed are but a small drop in the ocean of the research showing the multifarious benefits. The fact is, that it’s simply hard to over-egg (vegan alternative, of course!) the case for including flaxseed within one’s diet – especially if you’re completely plant-based and just want to ensure you get additional omega-3, along with walnuts.

So, why not make it a regular habit to include at least a tablespoon of flaxseeds in your daily diet?

Perhaps the best way to go about this is to have a supply always at the ready. Buy them whole in bulk. Buying pre-ground flaxseeds is much more expensive and it’s probably best to consume them within not too long a period of time after grinding – and you never know how long the ground version has been sitting on the shop shelf. So, possibly best to grind them yourself in a small coffee grinder and then store a kg of the ground up flaxseeds in a sealed container. So easy to dip into when you want. I also tend to make a weekly supply of muesli in a large container, into which I add ground flaxseeds from my 1kg flaxseed container. Since a tablespoon of flaxseeds weighs around 7 grams, I usually add around 100 grams for the week. Give it a good shake and you’re pretty confident about getting your weekly supply just from the muesli alone.

If it’s any help (although I’m not promoting either company), I buy flaxseeds in bulk (20 x 500 gram bags) from a company called Grapetree 65 . They appear to be one of the cheapest sources.

Additionally, I use a basic (but very effective) coffee grinder called the Duronic CG300 Electric Coffee Grinder Mill 66 , available from Amazon for £29.99. Of course, any coffee grinder will do the job. Just make sure you don’t grind the seeds too much (or you’ll get flaxseed butter) or too little (or you’ll leave intact and indigestible seeds). I tend to grind until the sound of the seeds hitting the top of the grinder stops, then scoop out the ground seeds.

References & Notes

  1. Olive Oil Injures Endothelial Cells []
  2. United States Department of Agriculture. Agricultural Research Service. USDA Food Composition Databases: Flaxseeds. []
  3. Pak J Pharm Sci. 2013 Jan;26(1):199-208. Flaxseed – a miraculous defense against some critical maladies. Akhtar S, Ismail T, Riaz M. [] []
  4. Can J Cardiol. 2010 Nov; 26(9): 489–496.The cardiovascular effects of flaxseed and its omega-3 fatty acid, alpha-linolenic acid. Delfin Rodriguez-Leyva, MD, PhD, Chantal MC Bassett, PhD, Richelle McCullough, BSc, and Grant N Pierce, PhD. []
  5. Contemp Clin Trials. 2011 May 17. The effect of dietary flaxseed on improving symptoms of cardiovascular disease in patients with peripheral artery disease: rationale and design of the FLAX-PAD randomized controlled trial. Leyva DR, Zahradka P, Ramjiawan B, Guzman R, Aliani M, Pierce GN. []
  6. Cancer Epidemiol Biomarkers Prev. 2008 Dec; 17(12): 3577–3587. Flaxseed Supplementation (not Dietary Fat Restriction) Reduces Prostate Cancer Proliferation Rates in Men Presurgery. Wendy Demark-Wahnefried, et al. []
  7. J Med Food. 2013 Apr; 16(4): 357–360. Flaxseed-Derived Enterolactone Is Inversely Associated with Tumor Cell Proliferation in Men with Localized Prostate Cancer. Maria Azrad, et al. []
  8. L. U. Thompson, J. M. Chen, T. Li, K. Strasser-Weippl, P. E. Goss. Dietary flaxseed alters tumor biological markers in postmenopausal breast cancer. Clin. Cancer Res. 2005 11(10):3828 – 3835 []
  9. Front Nutr. 2018; 5: 4. The Effect of Flaxseed in Breast Cancer: A Literature Review. Ana Calado, Pedro Miguel Neves, Teresa Santos, Paula Ravasco. []
  10. Nutr Metab (Lond). 2012; 9: 8. Flaxseed dietary fibers lower cholesterol and increase fecal fat excretion, but magnitude of effect depend on food type. Mette Kristensen, et al. []
  11. Rev Recent Clin Trials. 2015;10(1):61-7. Effect of flaxseed on blood lipid level in hyperlipidemic patients. Torkan M, Entezari MH, Siavash M. []
  12. J Res Med Sci. 2016; 21: 70. Published online 2016 Sep 1. The effect of flaxseed powder on insulin resistance indices and blood pressure in prediabetic individuals: A randomized controlled clinical trial Afrooz Javidi, et al. []
  13. Curr Pharm Des. 2016;22(2):141-4. Flaxseed and Diabetes. Prasad K, Dhar A. []
  14. Nutr Rev. 2018 Feb 1;76(2):125-139. Flaxseed supplementation on glucose control and insulin sensitivity: a systematic review and meta-analysis of 25 randomized, placebo-controlled trials. Mohammadi-Sartang M, Sohrabi Z, Barati-Boldaji R, Raeisi-Dehkordi H, Mazloom Z. []
  15. J Am Coll Nutr. 2017 Nov-Dec;36(8):646-653. Influence of Flaxseed Lignan Supplementation to Older Adults on Biochemical and Functional Outcome Measures of Inflammation. Di Y, et al. []
  16. ISRN Inflamm. 2013; 2013: 735158. Effect of L. usitatissimum (Flaxseed/Linseed) Fixed Oil against Distinct Phases of Inflammation. Gaurav Kaithwas, Dipak K. Majumdar. []
  17. Nutr Metab (Lond). 2018; 15: 36. A randomized trial of the effects of flaxseed to manage constipation, weight, glycemia, and lipids in constipated patients with type 2 diabetes. Noureddin Soltanian, Mohsen Janghorbani. []
  18. Obes Rev. 2017 Sep;18(9):1096-1107. The effect of flaxseed supplementation on body weight and body composition: a systematic review and meta-analysis of 45 randomized placebo-controlled trials. Mohammadi-Sartang M, et al. []
  19. Bioorg Med Chem Lett. 2016 Apr 1;26(7):1760-1. Cyclolinopeptides, cyclic peptides from flaxseed with osteoclast differentiation inhibitory activity. Kaneda T, Yoshida H, Nakajima Y, Toishi M, Nugroho AE, Morita H. []
  20. Pak J Biol Sci. 2008 Jul 1;11(13):1696-701. Preventive effects of flaxseed and sesame oil on bone loss in ovariectomized rats. Boulbaroud S, Mesfioui A, Arfaoui A, Ouichou A, el-Hessni A. []
  21. Nutrients. 2016 Mar; 8(3): 136. Effect of Flaxseed Intervention on Inflammatory Marker C-Reactive Protein: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Guan-Yu Ren, et al. []
  22. Int J Biol Macromol. 2015 Jan;72:614-23. Flaxseed lignan wound healing formulation: characterization and in vivo therapeutic evaluation. Draganescu D, et al. []
  23. J Clin Endocrinol Metab. 1993 Nov;77(5):1215-9. Effect of flax seed ingestion on the menstrual cycle. Phipps WR, Martini MC, Lampe JW, Slavin JL, Kurzer MS. []
  24. Non-Fish Sources of Omega-3 []
  25. Omega 3 Supplements = Snake Oil []
  26. Chia Seeds To The Rescue Of Type 2 Diabetics []
  27. Reprod. Nutr. Dev. 45 (2005) 581–597 581 Conversion of α-linolenic acid to longer-chain polyunsaturated fatty acids in human adults. Graham C. Burdge, Philip C. Calder. Institute of Human Nutrition, University of Southampton, Southampton, UK. []
  28. Polyphenols are collections of many (hence “poly-“) phenol structural units. Phenols are organic chemical compounds that have a pair of molecular groups stuck together – namely, a phenyl group with the molecular formula −C6H (six carbon atoms and one hydrogen atom) and a hydroxy group with the formula −OH (one oxygen atom and one hydrogen atom). When these bond together it forms a phenol with the formula C6H5OH. []
  29. Plant lignans include pinoresinol, lariciresinol, secoisolariciresinol, matairesinol, hydroxymatairesinol, syringaresinol and sesamin. []
  30. The other classes of phytoestrogens are isoflavones and coumestans. []
  31. Topic: Phytoestrogens. []
  32. Xenoestrogens are byproducts of the plastic and pesticide industries. Besides being a component of plastic, they are also found in conventional makeup/cosmetic products, household cleaners, laundry detergents, and some birth control medications. They are also found in sunscreens, chlorine and processed food. Naturally, with all this junk ending up in the oceans and rivers, fish become contaminated and people who eat fish thereby share in that contamination. []
  33. What’s the nutritional value of flaxseeds? []
  34. Wholism vs Reductionism – Not Just a War of Words []
  35. Sesamin is a lignan extracted from sesame seeds and a compound of sesame seed oil. A small amount is in flaxseeds. []
  36. Matairesinol is a plant lignan. It occurs with secoisolariciresinol in numerous foods such as oil seeds (including flaxseeds), whole grains, vegetables and fruits. []
  37. Pinoresinol is a lignan found in Styrax sp. and in Forsythia suspensa, as well as in the caterpillar of the cabbage butterfly, Pieris rapae where it serves as a defence against ants. It’s found in foods such as sesame seeds, Brassica vegetables, olive oil, and small amounts in flaxseeds. []
  38. Lariciresinol is a lignan, a type of phenylpropanoids. In food, it is found in sesame seeds and in Brassica vegetables. It is also found in the bark and wood of white fir. []
  39. Flaxseed Lignans: Biosynthesis, Metabolism, Antioxidant Activity, Bio‐Active Components, and Health Benefits. Alhassane Touré Xu Xueming. 29 April 2010. []
  40. Milder IE, Arts IC, van de Putte B, Venema DP, Hollman PC. Lignan contents of Dutch plant foods: a database including lariciresinol, pinoresinol, secoisolariciresinol and matairesinol. Br J Nutr. 2005;93(3):393-402. []
  41. Topic: Flax seeds. []
  42. There are websites that disagree with this, although there are few published studies showing negative effects, and those that do appear to relate more to consuming flax oil – usually called linseed oil. []
  43. Allergy Asthma Clin Immunol. 2010; 6(Suppl 2): P6. Flax seed allergy in children: an emerging allergen? Andrew O’Keefe, Sandeep Kapur, Gregory Rex, and Wade Watson. []
  44. J Cardiovasc Pharmacol. 2009 Nov;54(5):369-77. Flaxseed and cardiovascular health. Prasad K. []
  45. MayoClinic: Flaxseed and flaxseed oil. []
  46. J Food Sci Technol. 2014 Sep; 51(9): 1633–1653. Flax and flaxseed oil: an ancient medicine & modern functional food. Ankit Goyal, Vivek Sharma, Neelam Upadhyay, Sandeep Gill, Manvesh Sihag. []
  47. Oregon State University Linus Pauling Institute. Micronutrient Information Center: Lignans. []
  48. Two Types of Gut Bacteria: Plant Eaters’ & Meat Eaters’ []
  49. Dr. Greger’s Daily Dozen Checklist. Michael Greger M.D. FACLM March 30th, 2018 Volume 39 []
  50. Topics: Flax seeds. []
  51. Which Are Better: Chia Seeds or Flax Seeds? Michael Greger M.D. FACLM April 7th, 2017 Volume 35 []
  52. Flax Seeds for Hypertension. []
  53. Can Flax Seeds Help Prevent Breast Cancer? []
  54. Flax Seeds for Breast Pain. []
  55. Flax Seeds & Breast Cancer Survival: Clinical Evidence. []
  56. Flax Seeds & Breast Cancer Survival: Epidemiological Evidence. []
  57. Flaxseeds & Breast Cancer Prevention. []
  58. Just the Flax, Ma’am. Michael Greger M.D. FACLM August 22nd, 2007 Volume 1. []
  59. Flaxseeds vs. Prostate Cancer. []
  60. Flax Seeds vs. Diabetes. []
  61. Was It the Flaxseeds, Fat Restriction, or Both? []
  62. Flaxseeds for Sensitive Skin. []
  63. Flax Seeds vs. Chia Seeds. []
  64. Which Are Better: Chia Seeds or Flax Seeds? []
  65. Grapetree. Suppliers of flaxseeds. []
  66. Amazon: Duronic CG300 Electric Coffee Grinder Mill []

Why Whole Grains Are Better Than Flour

Okay, if you made bread from whole grains rather than floured grains, it would be a bit of a mess! However, there are compelling reasons why eating whole grains (wheat, barley, buckwheat, etc) provides far more health benefits than eating even the healthiest goods made with flour. And we’re not talking here about wholegrain1 as opposed to processed or refined grains – we’re talking about the whole grain – the complete edible part of the grain which has not been milled or ground down to millions of small particles, as happens when making any flour – be it wholegrain/wholemeal or highly refined (white flour).

The central message of this article concerns the different effects that grains and flours have inside your guts. First, though, a bit of background.

Anatomy of a grain

The above diagram shows the three parts of a grain:

  1. bran – the outer shell which protects the grain, containing most of the fibre
  2. endosperm – the major internal part providing food (energy) to the germ
  3. germ – the smaller internal part which provides the seed for future generations

What happens during flour milling?

When whole grains are milled to make refined flour, the bran and germ are removed, leaving only the endosperm. When whole grains are milled to make wholegrain flour, all three parts are ground down and made into a flour. Most people would have become aware that refined (white) flour is not as good for you as wholegrain flour, since the latter still provides some of the benefits of fibre, including:

  • helping to control blood glucose levels – thereby reducing sugar/insulin spikes
  • helping to maintain/ improve insulin resistance – a central feature of type 2 diabetes
  • increasing stool bulk – easing passage through the intestines and helping to prevent constipation
  • keeping you feeling full for longer
  • reducing blood cholesterol

Which grain has most fibre?

Just out of interest, the following is a list 2  of various grains, showing the average fibre content:

Take it out to put it back in

Vitamin E (a powerful antioxidant) 3 , B vitamins (essential for energy production, amongst other things) and trace minerals (including magnesium, selenium and zinc) 4  are partly destroyed by the time the final flour-based products have been baked. This is especially the case with ‘white’ flour (white because the darker-coloured fibre has been removed).

As an example, during milling, wheat loses 50% of its original phosphorus and calcium, 66% of iron, 50-70% of thiamine (vitamin B1)), 80% of niacin (vitamin B3), and 33% of tocopherol (vitamin E) 5 .

These and other nutrients – usually synthetic versions 6  – can then be added back into the final flour, thereby ‘enriching’ or ‘fortifying’ it. All well and good, but there’s plenty of strong evidence 7  suggesting, not only that the original nutrients combined within the actual plant (in this case, grains) are more effective than separately added vitamins and minerals, but studies 8  also show that some added ‘nutrients’ can be seriously harmful to health.

What else does commercially prepared flour contain?

I’m not even bothering to consider other flour products apart from bread (such as pies, pasties, cakes etc). The latter are generally so full of junk (whether animal- or plant-based) that, even if the pastry were of the highest possible quality, the product usually contains other ingredients than few WFPB nutritionists would recommend. However, if you’re determined to eat bread, the range of commercially produced offerings range from the reasonably okay to the downright awful.

Things to look out for, and, preferably, avoid:

  • salt 9
    • Dozens of similar studies demonstrate that if you reduce your salt intake, you may reduce your blood pressure. And the greater the reduction, the greater the benefit may be. But if you don’t cut down, chronic high salt intake can lead to a gradual increase in blood pressure throughout life.
  • sugar
    • some of my recipes contain a small amount, but commercial breads usually contain far too much
  • vegetable oils 10 11
    • Research confirms that ingestion of oil, no matter which type of oil or whether it was fresh or deep fried, showed a significant and constant decrease in arterial function.” 12
  • trans fats 13 14
    • trans fats (“partially hydrogenated” oils) are linked to serious health risks
  • potassium bromate (oxidising agent)
  • azodicarbonamide (dough conditioner/bleacher)
  • monoglycerides & diglycerides (emulsifiers E471)
  • butylated hydrocyanisole (BHA)
    • BHA is a preservative linked to cancer 15 16
  • caramel colouring
    • again, linked to increased cancer risk 17 18
  • high fructose corn syrup (HFCS)
    • HFCS is linked to kidney stones, metabolic syndrome, heart disease and diabetes 19 20 21 22
  • undeclared GMO soy oil 23
    • The bottom line is that there is no direct human data suggesting harm from eating GMOs, though in fairness such studies haven’t been done, which is exactly the point, critics counter. That’s why we need mandatory labelling on GMO products so that public health researchers can track whether GMOs are having any adverse effects.

And this isn’t a definitive list..

There have to be some benefits of refined flour…

Whilst there are no obvious health benefits to stripping whole grains of bran and germ, it does provide a longer shelf life. It also means the products ‘hit the sweet spot’ more quickly and can be a lot more addictive. The producers and retailers benefit when the consumer can’t resist another slice (or two) of the easily chewed and digested pap. So what if the blood glucose hits the roof? It’s well-known that when blood sugar levels rise quickly, they’ll drop just as quickly and result in rebound hunger. Your hunger won’t leave you alone.

Whole grains and the microbiome

This is the take-home bit of the blog. When you eat a milled grain, which consists of millions of tiny particles, most of it gets absorbed and digested well before it reaches your large intestine (the colon). However, when you eat a whole grain, chewing and digestion in the stomach and small intestine tend to leave much larger ‘chunks’ of grain that reach the colon.

So what?

In the colon, trillions of gut bacteria (the microbiota or gut flora) are waiting for these chunks of grain (prebiotics) so that they can further digest them and, thereby, release bi-products back into our bloodstream – bi-products which are of significant importance to our overall health – from reinforcing our immune system, protecting the endothelial cells of our blood vessels, to protecting us from mental depression.

The fascinating subject of gut bacteria has been covered in great detail in several previous blogs 24 25 26 27 . The chunks of whole grain act as prebiotics for our gut bacteria.

Final thoughts

So, if you want to provide valuable fuel for those little guys down there in your colon, stick to whole grains (boiled first, of course), and leave the bread, pasties, cakes, biscuits and other flour products on the shelf for the most part.

If you can’t live without bread, try to make it yourself. I’ve provided some really simple recipes 28 29 30 for a variety of bread types, each of which avoids the use of salt and oil. And if you can’t live without a bit of salt in your bread, then still best to make it yourself rather than buy commercially prepared bread.


  1. Wholegrain, wholewheat and wholemeal are all terms which tend to be used interchangeably to refer to the same thing. []
  2. Oldways Whole Grains Council: FIBER IN WHOLE GRAINS []
  3. The cereal grains: focus on vitamin E [2001]. Zielinski, H. Ciska, E. Kozlowska, H. []
  4. J Am Diet Assoc. 2001 Jul;101(7):780-5. The role of whole grains in disease prevention. Slavin JL, Jacobs D, Marquart L, Wiemer K. []
  5. White Enriched Bread vs. Whole Wheat Bread – Purdue e-Pubs. []
  6. Med Hypotheses. 2000 Dec;55(6):461-9. Natural vitamins may be superior to synthetic ones. Thiel RJ. []
  7. Vitamin C Supplements vs An Apple []
  8. How To Analyse the Health Claims Made for Dietary Supplements []
  9. Topics: salt. []
  10. CNS. Plant Oils Are Not a Healthy Alternative to Saturated Fat by T. Colin Campbell, PhD. July 21, 2016. []
  11. McDougall Newsletter August 2007. When Friends Ask: Why Do You Avoid Adding Vegetable Oils? []
  12. Topics: vegetable oil. []
  13. Vandana Dhaka, Neelam Gulia, Kulveer Singh Ahlawat, and Bhupender Singh Khatkarcorresponding. J Food Sci Technol. 2011 Oct; 48(5): 534–541. Published online 2011 Jan 28. doi: 10.1007/s13197-010-0225-8. Trans fats—sources, health risks and alternative approach – A review. []
  14. Trattner S, Becker W, Wretling S, Öhrvik V, Mattisson I. Food Chem. 2015 May 15;175:423-30. doi: 10.1016/j.foodchem.2014.11.145. Epub 2014 Dec 3. Fatty acid composition of Swedish bakery products, with emphasis on trans-fatty acids. []
  15. Otterweck AA, Verhagen H, Goldbohm RA, Kleinjans J, van den Brandt PA. Food Chem Toxicol. 2000 Jul;38(7):599-605. Intake of butylated hydroxyanisole and butylated hydroxytoluene and stomach cancer risk: results from analyses in the Netherlands Cohort Study. []
  16. []
  17. []
  18. Food caramels: a review – NCBI – NIH. []
  19. BMC Nephrol. 2018 Nov 8;19(1):315. doi: 10.1186/s12882-018-1105-0. Fructose increases risk for kidney stones: potential role in metabolic syndrome and heat stress. Johnson RJ et al. []
  20. Topics: High Fructose Corn Syrup. []
  21. Nutrients. 2017 Jan; 9(1): 11. High Dietary Fructose Intake on Cardiovascular Disease Related Parameters in Growing Rats. SooYeon Yoo, er al. []
  22. Glob Public Health. 2013;8(1):55-64. High fructose corn syrup and diabetes prevalence: a global perspective. Goran MI, Ulijaszek SJ, Ventura EE. []
  23. GMO Soy & Breast Cancer. Michael Greger M.D. FACLM November 17th, 2014 Volume 21. []
  24. Fibromyalgia, Probiotics & Gut Microbiota []
  25. Two Types of Gut Bacteria: Plant Eaters’ & Meat Eaters’ []
  26. Obstructive Sleep Apnea (OSA) & Gut Microbiota []
  27. Gut Microbiota & Depression []
  28. You Will Not Find A Simpler Bread Recipe []
  29. Yuri’s Wholesome Bread Recipe []
  30. Breads & Baking []

When the FUN is No Fun

It could be argued that the major nutritional problem experienced by those of us in ‘developed’ countries is an excess of macronutrients (particularly animal protein, saturated fat and sugar) plus salt. When this is combined, as it usually is, with a corresponding insufficient intake of micronutrients (minerals, vitamins, fibre and phytonutrients from fruit, veg, grains, legumes, nuts and seeds), then one descends the slippery slope towards truly unpleasant diseases and a likely early death.

Fatty under-nutrition

Whilst the term ‘over-nutrition’ is often used to define this modern dietary dilemma, it should really be thought of as ‘under-nutrition’, being that it’s too low in nutrients and too high in calories – a sort of nutrient starvation as the body expands. This is an utterly new paradox, probably never seen on this planet prior to the last few human generations.

When FUN is no fun

For the sake of clarity, I’m going to term this condition ‘Fatty Under-Nutrition’, or FUN for short.

The FUN starts young

The FUN starts early in life – even before birth. When women become pregnant, they’re usually urged to eat more because they’re “eating for two”, even though expectant and lactating mothers only require an additional 300 or so calories each day 1 . What all pregnant women really should watch is that they eat a healthy and varied diet, sufficient in macronutrients, but which includes all the micronutrients they and their baby need – notably, omega-3 fatty acids (DHA, in particular), iron, calcium, choline, iodine, vitamins C, D, B9 and, especially in the case of pregnant women eating a WFPB/vegan diet, plus sufficient vitamin B12 2 . Of course, any supplementation should always be in consultation with the medical professional (OB or GP) who is overseeing the pregnancy.

Excessive FUN, that is, a diet low in micronutrients but high in macronutrients (especially animal protein, saturated fat and sugar) during pregnancy can have a range of effects on the health of the mother and baby. The most obvious is excessively rapid weight gain in the mother. However, this factor alone has been shown 3 4 to:

  • increase the risk of labour induction
  • increase the risk of caesarean section
  • result in a higher birth weight
  • cause other complications during pregnancy and delivery

And it’s not just the mother

When infants and children are overfed, they can develop unhealthy dietary habits which may last a lifetime – being apparent in both their waistline and in the number of visits they need to make to their doctor and to the hospital later in life. Both quantity and type of food eaten in childhood can lead to metabolic implications with lifelong consequences.

Since mothers and expectant mothers want to do the very best for their children, they can be susceptible to over-feeding themselves and their babies in spite of their most loving and caring intentions. As one study stated: “In general, women are especially receptive to advice about diet and lifestyle before and during a pregnancy. This should be exploited to improve the health of future generations” 5 . Of course, in order to achieve this, the quality of the advice needs to be of the highest order.

In 2004, the American Dietetic Association pointed out that: “…the number of children who are overweight has more than doubled among 2- to 5-year-old children and more than tripled among 6- to 11-year-old children, which has major health consequences. This increase in childhood overweight has broadened the focus of dietary guidance to address children’s over consumption of energy-dense, nutrient-poor foods and beverages and physical activity patterns. Health promotion will help reduce diet-related risks of chronic degenerative diseases, such as cardiovascular disease, type 2 diabetes, cancer, obesity, and osteoporosis.” 6

A 2000 study stated that: “During early life and development the embryo, fetus and infant are relatively plastic in terms of metabolic function. The effect of any adverse environmental exposure is likely to be more marked than at later ages and the influence is more likely to exert a fundamental effect on the development of metabolic capacity” 7 . Whilst any baby, infant or young child faces health problems if they are significantly underweight, it’s increasingly understood that being overweight can be equally problematic – if not more so in some respects. 8 9 10

A 2005 review 11 concluded that: “Infants who are at the highest end of the distribution for weight or body mass index or who grow rapidly during infancy are at increased risk of subsequent obesity.

A 2006 study 12 showed that when a 4-month infant is fed more calories than recommended, it is a strong predictor of both increased weight gain before 2 years and increased risk of becoming obese in childhood and adulthood.

The take-home message of this is that parents and care-givers should choose foods that promote a healthy body weight and resist the temptation to ‘spoil’ with food or aim to promote the rapid growth of their child through overfeeding.

Teen FUN

An increasing percentage of adolescents are now over-weight. As of 2018, around a third of UK children between 2 and 15 are clinically obese13 , and US childhood obesity has more than doubled in the past 25 years 14 . Increases in pre-diabetes and full-blown type 2 diabetes (T2D) in childhood is just one disease correlated with childhood obesity 15 . Unless dietary changes are made, T2D symptoms are likely to remain and increase as these young people pass into adulthood. This is made more probable by the fact that the medical professions are slow to change from viewing T2D as a life-long, irreversible condition – thereby their efforts are aimed at merely ‘managing’ the disease, rather than viewing it as a completely reversible condition if appropriate dietary and lifestyle changes are made and adhered to. 16

Type 2 diabetes is rising rapidly in children and adolescents worldwide. Changing a child’s living environment to include physical activity, and a well balanced, low fat, high fiber diet, are important for the maintenance of a desirable body weight and improving insulin sensitivity…and decrease the risk of diabetes and cardiovascular disease.” 17

Fastest way to FUN

Just two words can sum up the major cause of FUN: ‘fast’ and ‘food’. Whether from take-aways, restaurants or supermarket shelves, fast food provides that perfect storm of high calories/low nutrients for children and adults alike.

One of the key findings of a 2018 study into fast food purchases for children by their parents in the US was:

Parents’ purchases of fast food for their children have increased in recent years:

  • In 2016, 91% parents reported purchasing lunch or dinner for their child in the past week at one of the four largest fast-food restaurants, on average twice per week. 
  • In contrast, 79% reported purchasing fast food for their child in the past week in 2010.” 18

As far back as 2003, a US report 19 indicated that fast-food use was reported by 42% of children, resulting in:

  • high intake of energy, fat, saturated fat, sodium, carbonated soft drinks, but
  • low intake of vitamins A and C, fruits and vegetables

FUN leads to yo-yo dieting

This problem becomes compounded when the adolescents try to lose weight by attempting various restrictive dieting regimes – most of which fail and many of which exacerbate existing and/or create new health problems.

Cross-sectional and prospective surveys have shown that a large percentage of adolescents, particularly females and even those of normal weight, diet at some time. While moderate changes in diet and exercise have been shown to be safe, significant psychologic and physiologic consequences may occur with extreme or unhealthy dieting practices. Moderate dieting has been shown to be associated with negative self-esteem in some adolescents. The very act of starting any diet increases the risk of eating disorders in adolescent girls. Extreme methods of weight loss can have adverse physiologic effects if not closely monitored. Electrolyte disturbances, cardiac dysrhythmias, and even sudden cardiac death can result from unhealthy or extreme dieting practices. Such practices are associated with other problem behavior in adolescents.” 20 .

A 2016 study 21 reported that, at any given time, more than 25% of male and around 60% of female adolescents are dieting in order to lose weight. In addition, up to 9% reported that they use maladaptive dieting habits, such as purging 22 .

Developing FUN in adulthood

It’s in so-called ‘developed’ countries that both children and adults are at particular risk from FUN.

Whilst a significant proportion (around 50%) of North Americans have inadequate intake of essential micronutrients and fibre, their energy balance is usually far in excess of physiological needs.  And it’s been known for some time that adults shouldn’t only be worried about this FUN leading to obesity and T2D:

Diet is estimated to contribute to about one-third of preventable cancers — about the same amount as smoking. Inadequate intake of essential vitamins and minerals might explain the epidemiological findings that people who eat only small amounts of fruits and vegetables have an increased risk of developing cancer. Recent experimental evidence indicates that vitamin and mineral deficiencies can lead to DNA damage.” 23

Energy density, portion size & availability

Standard foods, such as dairy, meat, sugar and vegetable oils tend to be more energy-dense in modern Western diets (often referred to as the SAD – Standard American Diet) when compared with the more traditional Asian and African diets, in which grains, legumes, and starchy vegetables play a much larger part.

Add to this the fact that, in Western societies, food portion sizes are larger and calorie dense/nutrient poor foods are much more easily available, and you have an adult population experiencing epidemic obesity-related diseases: coronary heart disease, hypertension, diabetes, and cancer. 24

FUN into old age – if you last that long…

As our populations reach advanced age, metabolic syndrome 25 is becoming the norm rather than the exception, with more than 40% of people in their 60’s and 70’s being affected 26 and, thereby, running a greater risk of dying prematurely 27 .

And dying isn’t even the worst of it. These chronic illnesses, during later years of one’s life, require regular hospitalisation, invasive, painful, and often humiliating medical procedures, restrictions of one’s privacy and independence, and severe limitations on the quality and enjoyment of one’s wise elderly years – years that should be active, happy and golden.

When the FUN stops

When you choose to eat a balanced WFPB diet, the FUN stops and the fun begins. Nutrient-rich foods become the norm and both micronutrients and macronutrients take care of themselves, with the ideal ratio of protein, fat and carbohydrate already wrapped up by nature with all the vitamins, minerals, phytochemicals and fibre that your body needs.

And no longer will you have to restrict how much you eat, nor worry about your weight, another paradox – albeit a very welcome one! – since, with such naturally healthy eating, you can’t help but get back to your ideal weight, thereby obviating the risk of falling into the cycle of yo-yo dieting.

Naturally, you’ll still be strongly advised to take B12 supplements and ensure you get enough sunlight, or else take vitamin D supplements; but apart from this, you can just concentrate on enjoying the rest of your life while your body and mind are naturally fuelled for optimal performance.

And all this by simply eating unadulterated plant foods…


  1. Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients) . Washington, DC: National Academies Press; 2005. []
  2. Piccoli, G., Clari, R., Vigotti, F., Leone, F., Attini, R., Cabiddu, G., … Avagnina, P. (2015). Vegan-vegetarian diets in pregnancy: danger or panacea? A systematic narrative review. BJOG: An International Journal of Obstetrics & Gynaecology, 122(5), 623–633. doi:10.1111/1471-0528.13280 []
  3. Maier JT et al: Antenatal body mass index (BMI) and weight gain in pregnancy – its association with pregnancy and birthing complications. J Perinat Med 44:397, 2016. []
  4. Kabiru W, Raynor BD: Obstetric outcomes associated with increase in BMI category during pregnancy. Am J Obstet Gynecol 191:928, 2004. []
  5. Roseboom TJ et al: Effects of prenatal exposure to the Dutch famine on adult disease in later life: an overview. Mol Cell Endocrinol 185:93, 2001 []
  6. Nicklas T, Johnson R, American Dietetic Association: Position of the American Dietetic Association: Dietary guidance for healthy children ages 2 to 11 years. J Am Diet Assoc 104:660, 2004 []
  7. Jackson AA: Nutrients, growth, and the development of programmed metabolic function. Adv Exp Med Biol 478:41, 2000. []
  8. N. Kapral, S. E. Miller, R. J. Scharf, M. J. Gurka, M. D. DeBoer. Associations between birthweight and overweight and obesity in school-age children. Pediatric Obesity, 2017 []
  9. Pediatr Obes. 2014 Apr;9(2):135-46. doi: 10.1111/j.2047-6310.2013.00155.x. Epub 2013 Apr 2. Socioeconomic status, infant feeding practices and early childhood obesity. Gibbs BG, Forste R. []
  10. Matern Child Nutr. 2013 Jan;9 Suppl 1:105-19. doi: 10.1111/mcn.12010. Nutrition in pregnancy and early childhood and associations with obesity in developing countries. Yang Z, Huffman SL. []
  11. Baird J et al: Being big or growing fast: systematic review of size and growth in infancy and later obesity. BMJ 331:, 2005 []
  12. Ong KK et al: Dietary energy intake at the age of 4 months predicts postnatal weight gain and childhood body mass index. Pediatrics 117:e503, 2006. []
  13. House of Commons Health Committee. Childhood obesity: Time for action. Eighth Report of Session 2017–19. Report, together with formal minutes relating to the report. Ordered by the House of Commons. 23 May 2018. []
  14. Baird J et al: Being big or growing fast: systematic review of size and growth in infancy and later obesity. BMJ 331:, 2005. []
  15. Whitlock EP et al: Screening and interventions for childhood overweight: a summary of evidence for the US Preventive Services Task Force. Pediatrics 116:e125, 2005 []
  16. Diet Reverses Type 2 Diabetes – How Long Have We Known This? []
  17. Vivian EM: Type 2 diabetes in children and adolescents–the next epidemic? Curr Med Res Opin 22:297, 2006 []
  18. UConn Rudd Center for Food Policy and Obesity. Parents’ report of fast-food purchases for their children: Have they improved? September 2018. []
  19. Paeratakul S et al: Fast-food consumption among US adults and children: dietary and nutrient intake profile. J Am Diet Assoc 103:1332, 2003 []
  20. Starling P et al: Fish intake during pregnancy and foetal neurodevelopment–a systematic review of the evidence. Nutrients 7:2001, 2015 []
  21. Zullig KJ, Matthews-Ewald MR, Valois RF: Weight perceptions, disordered eating behaviors, and emotional self-efficacy among high school adolescents. Eat Behav 21:1, 2016 []
  22. Purging – a practice known as bulimia – oscillates with bingeing and can result in a wide range of health issues, including rupture of the oesophagus or stomach, dental and oral damage due to stomach acid exposing during vomiting. []
  23. Ames BN, Wakimoto P: Are vitamin and mineral deficiencies a major cancer risk? Nat Rev Cancer 2:694, 2002 []
  24. Isganaitis E, Lustig RH: Fast food, central nervous system insulin resistance, and obesity. Arterioscler Thromb Vasc Biol 25:2451, 2005 []
  25. Metabolic syndrome is a combination of central obesity, dysglycaemia, dyslipidemia and arterial hypertension. Most of the disorders associated with metabolic syndrome have no visible symptoms except for a large waist circumference. Additional symptoms include increased thirst and urination, fatigue, and blurred vision. []
  26. Arq Bras Cardiol. 2014 Mar; 102(3): 263–269. Prevalence of Metabolic Syndrome in Elderly and Agreement among Four Diagnostic Criteria. Maria Auxiliadora Nogueira Saad et al. []
  27. Firdaus M: Prevention and treatment of the metabolic syndrome in the elderly. J Okla State Med Assoc 98:63, 2005 []

Ghrelin & Obesity – A Tentative Step Through the Minefield

Increased appetite is a driving force for weight gain, and unchecked weight gain does, of course, lead to obesity. There’s a growing body of literature suggesting that ghrelin, the so-called hunger hormone” or “starvation hormone”, plays an important role in appetite fluctuations. Whilst we looked at leptin, the “satiety hormone” in the previous blog 1 , this one is an analysis of some research on ghrelin and obesity 2 .

Because this is a rather complex blog, technical terms are in green – either click associated number to go to References/Notes section (blue arrow returns to same place in the text), or hold cursor over relevant number to reveal contents.

What is ghrelin?

The complexity of this topic starts as soon as one looks for the derivation of the word “ghrelin”, with some authorities 3 stating that it’s derived from “ghre” (grow) and “relin” (release), while another authorities4 appear to relate its etymological roots to the use of letters from its understanding as a “Growth Hormone RELease INducing” hormone. In any case, it is agreed that it was first isolated and identified by Kojima and Kangawa et al in 1999 5 . Three years later, its specific brain receptor, GHS-R 1a, was also identified 6 .

Whilst leptin is mainly secreted by fat cells 7 and insulin is secreted by beta cells in the islets of Langerhans within the pancreas, ghrelin is primarily secreted from cells in the stomach (see below for more detail on this).

Ghrelin vs leptin

Having already looked at leptin in the previous blog, it’s worth starting by drawing comparisons between it and ghrelin, since they are regarded as working together (although in opposite directions) to help regulate appetite and metabolism.

Ghrelin and leptin are the two hormones 8 that are most responsible for regulating appetite – to ensure you don’t eat too few calories and starve to death while also ensuring you don’t eat too many calories and become obese. Well, that’s the hope anyway!

As an appetite stimulant, ghrelin is called an orexigenic hormone9 that stimulates food intake and thereby helps regulate body weight, while the appetite-inhibiting hormone leptin is known as an anorexigenic hormone 10

They are both homeostatic 11  hormones which means they are going to act on the hypothalamus 12 , the part of the brain that maintains the body’s internal balance (homeostasis).

The hypothalamus acts as the link between the endocrine 13 and nervous 14 systems. The hypothalamus produces releasing and inhibiting hormones, which stop and start the production of other hormones throughout the body.

Ghrelin and leptin act on different parts (receptors) within the hypothalamus.

Ghrelin acts on the lateral 15  hypothalamic brain cells16 , while leptin acts on the ventromedial 17 hypothalamic brain cells.

Ghrelin makes you Grow” – makes you eat, while “Leptin makes you Lean” – makes you stop eating. These are two mnemonics that might help to remember which is which.

Ghrelin is the only peripheral 18 orexigenic hormone that activates receptors found in the appetite centre – viz. the hypothalamus and pituitary gland.

Ghrelin is produced by endocrine cells 19 of the oxyntic glands20 within the gastric fundus21 . It’s also secreted, to a lesser extent, by the body of the stomach, the mucosa of the duodenum and jejunum 22 , the lungs, the urogenital organs, and the pituitary gland.

Stomach distension reducing ghrelin-production and inhibiting appetite.

Once produced in the stomach, ghrelin is released into the bloodstream, passes through the blood-brain-barrier 23 to the lateral hypothalamus, and causes a hunger response.

Ghrelin will also have an effect on the stomach itself, causing an increase in gastric acid production and gastric motility 24 . This prepares the stomach for the food that’s been anticipated by the brain. Daily habits (breakfast, lunch and dinner) become ingrained so that our ghrelin production starts to increase before we’re even consciously aware that we’re hungry.

Ghrelin stimulants (or inducers) include hypoglycaemia (low blood glucose), an empty stomach, and low body weight (low body fat content).

Ghrelin suppressants (or inhibitors) include activation of the stomach’s stretch receptors as the stomach becomes full of food (stomach distension).

Leptin, on the other hand, is primarily produced by white adipose tissue.

As the fat cells increase in size, they produce more leptin. A negative feedback signal 25 is caused when leptin travels from the fat cells, through the bloodstream and blood-brain-barrier to the ventromedial hypothalamic cells in the hypothalamus – reducing appetite and food intake. Ideally, this means that fat controls its own levels within the body. 26

Inducers for leptin include insulin and emotional stress. Below, we consider how modern dietary changes may have messed with the normally healthy relationship between stress and hunger hormones.

Leptin and insulin share common effects in controlling food intake and energy metabolism, with each playing an important role in blood glucose homeostasis. They directly regulate each other: leptin inhibits insulin and insulin stimulates leptin synthesis and secretion.

Note: ANS = Autonomic Nervous System.

Leptin increases insulin sensitivity 27 , in part, by decreasing adiposity and lipotoxicity 28 . Leptin decreases hepatic (liver) production of glucose – glycogenolysis 29 – contributing to its glucose-lowering effects. 30

Studies have revealed that leptin has the effect of normalising hyperglycaemia 31 and hyperinsulinaemia 32 . It’s also clear 33 that levels of both need to drop for fat burning – i.e. gluconeogenesis 34 – to commence.

Whilst it would seem intuitively obvious in evolutionary terms that when the body is under stress (fight or flight), appetite for food would be switched off – perhaps causing the production of leptin to achieve this, studies 35 have pointed out a complication in the modern world with psychological stress: namely, that it often results in “comfort eating” (usually fatty, sweet, high calories foods). The latter modern habit can confuse the picture.

The previous blog pointed 1 out the paradox that obese humans tend to have higher levels of leptin – the hunger-inhibiting hormone – suggesting they have developed leptin resistance. This results in a toxic cycle of increased leptin insensitivity leading to increased leptin levels (irrespective of insulin and ghrelin levels) leading to increased amounts of fat being stored in the body, leading to the fat cells producing even more leptin.

To test the latter, researchers intravenously increased leptin levels during times of emotional stress in order to see whether this would lower the compensatory intake of such comfort food. They concluded that “…initial findings suggest that acute changes in leptin [i.e. increasing it in the short term] may be one of the factors modulating down [reducing] the consumption of comfort food following stress.” 36

A major inhibitor of leptin is short term fasting. When you haven’t eaten for several hours, leptin levels should drop and ghrelin levels should rise. A theory which appears to work okay in healthy, non-obese individuals.

Active & inactive ghrelin

The acylation of inactive (non-acyl) to active (acyl) ghrelin.

There are several different forms of ghrelin, but the main two are called the “inactive” (des-acyl ghrelin) and “active” (acyl ghrelin – a peptide of 28 amino acids) forms. The inactive form accounts for more than 90% circulating within the bloodstream 37 . However, the inactive form has to be converted into the active form in order to do its work as an appetite stimulant. It does this via an enzyme called ghrelin O-acyltransferase or GOAT 38 39  . This process is critical both for the orexigenic and the gastric-emptying actions of ghrelin.

How ghrelin exerts its effect on the body

There are various possible actions by which ghrelin exerts its effect within the body, including:

  • overproduction/underproduction of ghrelin before and/or after meals
  • increased/decreased receptor sensitivity to ghrelin action

Ghrelin & positive feedback

The appetite-generating effect of ghrelin can be described as a direct positive feedback loop40  which maintains increased activity of AgRP neurons 41 so as to drive feeding behaviour until satiety is reached 42 , when leptin kicks in to do its job of suppressing appetite.

Other physiological functions of ghrelin

The discovery of the GOAT enzyme revealed that ghrelin is involved in many additional physiological functions, ranging from regulation of the immune and cardiovascular systems, up-regulation of insulin-like growth factor (IGF-1), to a dominant role in the gastrointestinal system and involvement in gastric emptying and intestinal motility 43 .

Although it has a role as a growth factor secretagogue 44 , stomach-derived ghrelin doesn’t appear to be necessary for growth and appetite stimulation, since ghrelin-deficient animals still appear to grow and eat quite normally 45 .

There must, therefore, be some form of redundancy within the body – that is, other physiological processes that promote growth and appetite which are able to compensate for the absence of ghrelin.

Actions and therapeutic pathways of ghrelin for gastrointestinal disorders

As can be seen in the diagram, ghrelin affects multiple systems. Whilst being secreted mainly by the stomach, it has effects in multiple areas, including the CNS (central nervous system), the immune system, the adrenal gland and the cardiovascular system. It can also affect the proliferation of osteoblasts 46  and neoplastic cells 47 .

Ghrelin, obesity & appetite

The precise role of ghrelin in the pathophysiology of obesity is still under investigation. It’s considered by some that if we’re able to get a firm grip on how ghrelin initiates appetite, then increasing its level could be a revolutionary new method of obesity management and treatment.

The role of ghrelin in the development of obesity.

Reduced postprandial suppression of ghrelin in obese individuals

In a number of studies of obese adults and obese children 48 49 , it’s been reported that postprandial suppression of ghrelin is lower in such obese groups compared to controls with normal body mass index (BMI).

This makes it a reasonable assumption that higher consumption of food by obese individuals is linked to a continuing feeling of hunger, even after consuming a meal with sufficient caloric content to satisfy their physiological needs. These findings have supported the ‘disease pattern’ of obesity which has underlying mechanisms and causes like other common disorders.

What’s the problem with ghrelin in relation to obesity?

So, is the obesity-ghrelin problem (and, by inference, the insulin-ghrelin problem) a matter of an overproduction of ghrelin or is it similar to what we’ve seen with leptin and insulin – i.e. insensitivity leading to resistance?

Since studies (mentioned above) 45 have shown that animals completely deficient in ghrelin can still grow normally without becoming obese, it would seem that the likeliest problem is the overproduction of ghrelin (regardless of the how much food is consumed) rather than a ghrelin insensitivity or oversensitivity.  Various studies support this hypothesis 50 51 52 , although uncertainty still remains regarding the precise mechanism/s involved, which range from a possible dysfunction in the gene for ghrelin to the production of antibodies to the peptide receptors which antagonise 53 ghrelin’s effects which, in turn, might lead to disturbances in the production and actions of ghrelin. Additionally, interactions with other hormones (insulin, growth hormone (GH), etc)  are likely to account for at least some of the ghrelin-obesity anomalies.

We still don’t fully understand the relationship between ghrelin and insulin – a relationship which appears to be based on an overproduction of ghrelin leading to a similar overproduction and eventual insensitivity/resistance to insulin 54 .

The view that the obesity-ghrelin problem is not due to an overproduction of ghrelin in obese individuals is supported by many studies. showing that the mean serum ghrelin level is generally lower in obese patients compared to lean individuals 55 56 , although the number of ghrelin-producing cells was found to be more abundant in the fundus of morbidly obese patients.

You’d be excused for expecting obese individuals to have lots more of this appetite-promoting hormone floating around their bloodstream than would non-obese individuals, given that the former continue eating beyond their physiological needs. And you wouldn’t be alone. The following graph 57  reveals that, though ghrelin levels rise in expectation of a meal and fall after that meal in both obese and non-obese individuals, the levels of ghrelin are consistently higher in non-obese than in obese individuals.

A further study concluded: “Contrary to our hypothesis, however, obese subjects have lower plasma concentrations of the adipogenic 58 hormone ghrelin than age-matched lean control subjects.” 59

The same study made some suggestion about what’s actually happening with ghrelin in obese individuals, suggesting that it may be a downregulation 60 of ghrelin as a consequence of elevated insulin or leptin, because fasting plasma ghrelin levels are negatively correlated with fasting plasma levels of insulin and leptin.

They also speculated that decreased secretion of ghrelin could be responsible for decreased levels of circulating growth hormone (GH) 61 in obese individuals 62  .

Ghrelin, growth hormone (GH), diabetes & obesity

Ghrelin, as stated above, causes the release of growth hormone (hence the proposed origin of its name – Growth Hormone Release Inducing hormone). The relationships between obesity, adipose tissue, GH and ghrelin make an already complex situation even more complex.

Obesity induces hyperinsulinaemia, hypoadiponectinaemia 63 , hyperleptinaemia 64 , reduced serum ghrelin, and increased free fatty acid levels. The effect of this is that GH secretion from the pituitary gland is suppressed 65 .

But what’s the relationship between low levels of GH and ghrelin in obese/diabetic individuals?

Insulin resistance is highly associated with visceral obesity, non-alcoholic liver disease, and type 2 diabetes. In turn, all these conditions are associated with low GH secretion. Since high levels of GH are likely to contribute to the development of insulin resistance when, that is, caloric intake is greater than physiological demand (when you eat more calories than you burn), the body’s reduction in GH secretion in obesity may be an adaptive phenomenon which is aimed at preventing insulin resistance occurring.

However, a problem occurs with this situation: namely, when GH secretion is reduced, it’s likely to lead to further increases in fat accumulation by reducing the process of lipolysis 66 . It’s clear to see how this increased retention of fat can exacerbate obesity and establish a dangerous vicious circle. Indeed, truncal adiposity 67  is one of the most important clinical findings of a condition known as adult GH deficiency syndrome (GHD) 68 .

So, when levels of circulating GH are reduced, as they are in cases of obesity, it’s proposed 59 that decreased plasma ghrelin concentrations – which are seen in obesity – represent a physiological adaptation to the positive energy balance 69 associated with this disease.

GH (like insulin) is essential in adapting the utilisation of calories to the amount of ingested food, promoting anabolism 70 in the case of positive energy balance, with catabolism 71 occurring in the case of negative energy balance 72 . While insulin is the main metabolic hormone in the fed state (positive energy balance), GH assumes a key role as stimulator of lipolysis during prolonged fasting (negative energy balance), when it causes preferential oxidation of lipids and protein synthesis 73 .

The increase in GH secretion that occurs with fasting may have represented an evolutionary advantage in times of food scarcity. However, GH and IGF-I have opposite effects on glucose homeostasis, with the former reducing insulin sensitivity (mainly acting in the liver) and the latter increasing it in the muscle.” 74

Plenty more detail on the relationship of ghrelin and GH is available in a number of excellent studies 75 .

Ghrelin and diets

As you’d expect, levels of ghrelin increase during dieting. This could explain why it’s very difficult to achieve long-term success from dieting. 76 77

Two way to manage obesity

There are two main approaches in managing obesity:

  • conservative – e.g. diet, exercise and lifestyle changes
  • surgical – through various weight-loss surgical procedures, widely known as bariatric surgery

The conservative ways of preventing and treating diabetes, primarily through dietary changes, have been covered in such detail in previous blogs 78 79 80 81 that we hardly need to repeat them here.

Ghrelin & bariatric surgery

It’s clear that bariatric surgery is going to cause some purely mechanical effects (less room for food) that would be responsible for subsequent increased food restriction, as well as often leading to malabsorption 82 . After all, the person concerned has had bits of their guts removed and/or joined together. However, during the past couple of decades, the identification of significant humoural 83 changes (that lead to less hunger or earlier satiety postprandially) has complicated the picture of why appetite changes occur after such surgical procedures 84 48 .

Ghrelin & two types of bariatric surgery

Researchers have recently tried to explain the impressive results of bariatric surgery in terms of weight loss by evaluating the changes in ghrelin concentration following roux-en-y gastric bypass (RYGB) 85 and especially sleeve gastrectomy (SG) 86 . In the latter procedure, the gastric fundus, where most ghrelin is produced, is totally removed. A recent meta-analysis 51 showed that the ghrelin level does fall significantly following SG. In patients who undergo RYGB, the results of various studies are contradictory 87 .

Does bariatric surgery work?

Both these techniques lead to exceptionally good results in weight loss. Based on the fact that, anatomically, SG is purely restrictive compared to RYGB, which additionally creates malabsorption by the rapid shunt of undigested food to the distal small intestine 88 , the role of ghrelin is now being investigated more than ever. Whether or not bariatric surgery works, we know that even morbidly obese individuals can return to a normal healthy weight without the need for such extreme dietary measures 89 . Additionally, once the body is back to a healthy homeostatic state, one would assume that ghrelin levels would also normalise.

Ghrelin & age-related obesity

The adjacent graph 90 shows that ghrelin levels decrease with age, backed up by other studies 91 . This would be in line with the fact that ageing is accompanied by a decrease in both energy expenditure and locomotor activity – with decreases in muscle strength and endurance leading to functional decline. The latter factors, taken in isolation, would imply that there would be a corresponding increase in body weight, particularly in the form of fat.

This has an effect on food intake as well as energy expenditure, thereby potentially preventing the development of age-related obesity. 92

Ghrelin and anorexia

Due to the proven relationship of ghrelin with appetite, researchers are also investigating the potential connection of ghrelin to anorexia. Insight into the modification of the endogenous ghrelin system seems to be promising not only for the control of obesity, but also for the management of clinically significant anorexia and pathological weight reduction.

Does anorexia produce ghrelin insensitivity?

Accumulating evidence has shown that in patients with anorexia nervosa, there’s a paradoxical increase in plasma ghrelin level even when compared with matched controls or obese patients 93 , suggesting that the situation may be one of ghrelin-insensitivity 94 .

Ghrelin – homeostatic and non-homeostatic feeding

Anorexia nervosa, bulimia nervosa 95 and other eating disorders appear to have pathophysiologies 96 linked to dysfunctions of reward mechanisms. 97 Additional research 98  supports the hypothesis that ghrelin doesn’t just increase appetite by homeostatic need – that is, feeding driven by a metabolic need where hormones “speak to one another” in order to create homeostatic balance, but also by non-homeostatic feeding  – that is, feeding driven by non-metabolic factors, such as reward (“hedonic feeding” 99 ) and memory. The latter factors have less to do with the body trying to reach homeostatic balance than with emotional, psychological and social factors.

Tail wagging the dog

The huge increase in the consumption of ultra-processed foods (high in sugar/fat/calories and low in nutrients) could be regarded as a causal factor in the dysregulation of homeostatic hormonal systems (ghrelin, leptin, insulin, etc), resulting in the tail (learned emotional need) wagging the dog (actual physiological need).  This results in our medical professions struggling to cope with the ever-increasing effects of diet-related diseases, and in millions of suffering people who end up with diseased bodies and shortened lives.

Cancer and ghrelin administration

Ghrelin and cancer.

In vitro studies 100  have documented that both intra-peritoneal 101 and systemic 102 administration of ghrelin have the potential of improving appetite and nutritional status, and at the same time reducing the metabolic rate in patients with end-stage cancer.

This research suggests a likelihood that additional gastric disorders (e.g. gastritis, GI tract carcinoma, and other functional GI disorders) disrupt the morphological structure 103 of the stomach, and thus alter ghrelin production – being that the stomach is its major source. “These alterations may induce various GI disorders including functional GI disorders, eating disorders, abnormal energy homeostasis and growth. By understanding ghrelin secretion in the regulation of GI disorders, ghrelin levels may serve as a good diagnostic biomarker for early detection of GI disorders.” 100

The roles that ghrelin may play in relation to cancer is still relatively unclear. One study concludes: “It is currently unclear whether the ghrelin axis has tumor-promoting effects, or indeed whether it may inhibit tumorigenesis in vivo, and further studies are therefore required to elucidate its role in cancer.” 104

Limitations of Studies Investigating Ghrelin

There are several limitations in investigating ghrelin:

  • very small number of studies and RCTs (randomised controlled trials)
  • there are two forms of circulating ghrelin, inactive ghrelin (90%), and active acylated ghrelin (10%) 50 and published studies tending to measure total rather than active ghrelin levels
  • the active form of ghrelin has been reported to be unstable at room temperature
  • there’s a current lack of standardisation in ghrelin measurement in terms of timing of sample collection, collection method, follow-up period, sample storage, and the radioimmunoassays 105 being used

The latter issues make precise measurement a challenge and this may be an issue in the reproducibility of results in the future.

Prader-Willi syndrome (PWS)

PWS, a congenital form of obesity, is caused by a mutation on chromosome 15. One of the effects of this is that ghrelin levels are hugely increased and the individual is forever hungry. If untreated, eating far, far too much – resulting in morbid obesity. It’s thought 106 that elevated ghrelin levels in PWS children precede the onset of obesity.

Prader-Willi syndrome.

Prader-Willi syndrome vs non-congenital obesity

When ghrelin levels were compared between children with PWS and children with non-congenital obesity (i.e. nothing wrong with their chromosome 15), it was found 107 that, even immediately after eating meals, ghrelin levels remained comparatively much more elevated in the PWS children.

The reason for this is speculated 108  to be that hyperghrelinaemia 109 in early infancy might be a response to the failure to thrive, and that chronic or persistent hyperghrelinaemia eventually promotes hyperphagia (overeating) in early childhood. 110

Once again, it would appear that more complexity has befallen us, since the obesity in PWS individuals is accompanied by elevated levels of ghrelin in the blood, while in non-congenitally obese individuals, ghrelin levels appear to be reduced even compared with non-obese individuals.

Further research on ghrelin

Whilst ghrelin research is ongoing, and all will hopefully be made clearer in the near future, a two-part YouTube video 111 112 presents a very detailed analysis of the discovery of ghrelin and its receptor, along with its relationship to GH and its role in starvation-prevention.

Final thoughts

The above is by no means a comprehensive analysis either of the specific role/s of ghrelin in the development of obesity nor of its other varied physiological roles. Indeed, I haven’t even touched on another important appetite-suppressing hormone, namely PYY 113 . Its relationship with ghrelin and other hormones is sufficiently complex to warrant a separate analysis, although there are plenty of studies for the interested reader. 114 115 116

What is clear, though, is that ghrelin appears to be attracting attention with regard to the treatment of obesity.

However, it does continue to be a source of irritation that, within the realm of medical research, so much emphasis is directed towards treatment (usually through searches for pharmaceutical and/or gene-based solutions) rather than prevention. And, as strong evidence suggests, obesity is best treated through dietary change; with the most effective and long-lasting dietary change being one that increases the ratio of whole plant foods to processed and/or animal foods 117 118 119 .

My expectation is that most research dollars will be spent on developing highly-profitable pharmaceutical solutions for perceived problems that relate to ghrelin and associated hormones. The elephant in the room is dietary change, of course. When we looked at toxic hunger vs real hunger 120 , we merely touched on the issue of ghrelin. However, it would seem relevant to this discussion to consider that eating a WFPB diet – which has significant impact on both homeostatic (the physiological effects of hormones, etc) and non-homeostatic feeding (‘comfort eating’ and ‘addictive’ dietary habits) – would also have direct and/or indirect effects on the effectiveness of the ghrelin-leptin-insulin-GH axis. Once again, more research is needed in this area, although where the research dollars come for this type of research is likely to be an ongoing problem.

References & Notes

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  9. Orexigenic – An orexigenic, or appetite stimulant, is a drug, hormone, or compound that increases appetite and may induce hyperphagia – overeating. This can be a naturally occurring neuropeptide hormone such as ghrelin, orexin or neuropeptide Y, or a medication which increases hunger and therefore enhances food consumption. []
  10. Anorexigenic – an anorexigenic hormone reduces or inhibits appetite. []
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