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

  1. Leptin – The “Fat” Hormone? [] []
  2. In Vivo. 2017 Nov-Dec;31(6):1047-1050. Ghrelin and Obesity: Identifying Gaps and Dispelling Myths. A Reappraisal. Makris MC, Alexandrou A, Papatsoutsos EG, Malietzis G, Tsilimigras DI, Guerron AD, Moris D. []
  3. Walker A K, Gong Z, Park W M, Zigman J M, Sakata I. Expression of Serum Retinol Binding Protein and Transthyretin within Mouse Gastric Ghrelin Cells. PLoS One. 2013;8:e64882. []
  4. Open University: The Science of Nutrition& Healthy Eating. []
  5. Methods Enzymol. 2012;514:3-32. doi: 10.1016/B978-0-12-381272-8.00001-5. History to the discovery of ghrelin. Bowers CY. []
  6. Hormones (Athens). 2016. Effects of ghrelin in energy balance and body weight homeostasis. Mihalache L, Gherasim A, Niţă O, Ungureanu MC, Pădureanu SS, Gavril RS, Arhire LI. []
  7. Leptin is mainly secreted by adipocytes (fat cells) of white adipose tissue. It’s also produced in brown adipose tissue, placenta syncytiotrophoblasts, ovaries, skeletal muscle, the lower part of the fundic glands within the stomach, mammary epithelial cells, bone marrow, gastric chief cells and P/D1 cells. []
  8. A hormone is any member of a class of signalling molecules produced by glands in multicellular organisms that are transported by the circulatory system to target distant organs to regulate physiology and behaviour. []
  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. []
  11. Homeostasis is the state of steady internal conditions maintained by living things. This dynamic state of equilibrium is the condition of optimal functioning for the organism and includes many variables, such as body temperature, fluid balance, blood sugar levels, and body weight being kept within certain pre-set limits. []
  12. The hypothalamus is an endocrine gland. Endocrine glands within the endocrine system secrete their products, hormones, directly into the blood rather than through a duct. The major glands of the endocrine system include the pineal gland, pituitary gland, pancreas, ovaries, testes, thyroid gland, parathyroid gland, adrenal glands and, of course, the hypothalamus. []
  13. The endocrine system is a chemical messenger system consisting of hormones, the group of glands of an organism that secrete those hormones directly into the circulatory system to regulate the function of distant target organs, and the feedback loops which modulate hormone release so that homeostasis is maintained. []
  14. The nervous system is the part of an animal that coordinates its actions by transmitting signals to and from different parts of its body. The nervous system detects environmental changes that impact the body, then works in tandem with the endocrine system to respond to such events. []
  15. Lateral means of, at, towards, or from the side or sides. The green cells on the diagram. []
  16. specifically, on the cell receptor known as the ghrelin/growth hormone secretagogue receptor or GHS-R. Secretagogue receptors are those that promote secretion. []
  17. Ventral means on or relating to the underside of an animal, plant or object – in this case the brain; while ventromedial indicates that it’s situated towards the middle of the ventral part. The red cells on the diagram. []
  18. Peripheral – that is, produced or taking place outside of the central nervous system , CNS – i.e. outside the brain and spinal cord []
  19. International Journal of Peptides. Volume 2010, Article ID 945056, 7 pages. Ghrelin Cells in the Gastrointestinal Tract. Ichiro Sakata, Takafumi Sakai. []
  20. Oxyntic glands – these are made up of secretory cells which produce hydrochloric acid in the main part of the stomach, or the glands which they compose []
  21. the upper part of the stomach, which forms a bulge above the level of the opening of the oesophagus, furthest from the pylorus []
  22. Duodenum and jejunum are the first and second parts of small intestine, with the ileum being the final part before entering the large intestine, the colon. []
  23. The blood-brain barrier is a semipermeable membrane separating the blood from the cerebrospinal fluid, and constituting a barrier to the passage of cells, particles, and large molecules. Only specific substances, including ghrelin, are able to pass through this barrier. []
  24. Gastric or gastrointestinal motility is defined by the movements of the digestive system, and the transit of the contents within it. []
  25. A negative feedback (or balancing feedback) signal occurs when some function of the output of a system, process, or mechanism is fed back in a manner that tends to reduce the fluctuations in the output, whether caused by changes in the input or by other disturbances. []
  26. (Morton G. J., Schwartz M. W. (2011). Leptin and the central nervous system control of glucose metabolism. Physiol. Rev. 91, 389–411. []
  27. Kamohara S., Burcelin R., Halaas J. L., Friedman J. M., Charron M. J. (1997). Acute stimulation of glucose metabolism in mice by leptin treatment. Nature 389, 374–377 10.1038/38717 []
  28. Lipotoxicity is a metabolic syndrome that results from the accumulation of lipid intermediates in non-adipose tissue, leading to cellular dysfunction and death. The tissues normally affected include the kidneys, liver, heart and skeletal muscle. []
  29. Glycogenolysis is the breakdown of the molecule glycogen into glucose, a simple sugar that the body uses to produce energy. The opposite of glycogenolysis is glycogenesis, which is the formation of glycogen from molecules of glucose. []
  30. Indian J Endocrinol Metab. 2012 Dec; 16(Suppl 3): S549–S555. Leptin therapy, insulin sensitivity, and glucose homeostasis. Gilberto Paz-Filho, Claudio Mastronardi, Ma-Li Wong, and Julio Licinio. []
  31. Hyperglycaemia is an excess of glucose in the bloodstream, often associated with type 2 diabetes, also known as diabetes mellitus. []
  32. Hyperinsulinaemia is a condition in which there are excess levels of insulin circulating in the blood relative to the level of glucose. While it is often mistaken for diabetes or hyperglycaemia, hyperinsulinemia can result from a variety of metabolic diseases and conditions. []
  33. Cell. Volume 172, issue 1, P234-248.E17, January 11, 2018. Leptin Mediates a Glucose-Fatty Acid Cycle to Maintain Glucose Homeostasis in Starvation. Rachel J. Perry et al. []
  34. Gluconeogenesis is is a metabolic pathway that results in the generation of glucose, to be burned as energy, from certain non-carbohydrate carbon substrates, including fat and protein. []
  35. Physiol Behav. 2012 Aug 20; 107(1): 34–39. Leptin concentrations in response to acute stress predict subsequent intake of comfort foods. A. Janet Tomiyama et al. []
  36. Physiol Behav. 2012 Aug 20;107(1):34-9. Leptin concentrations in response to acute stress predict subsequent intake of comfort foods. Tomiyama AJ et al. []
  37. Total and active ghrelin levels in women with polycystic ovary syndrome. S. Ferrero P. Anserini V. Remorgida G. Bentivoglio N. Ragni. Human Reproduction, Volume 21, Issue 2, 1 February 2006, Pages 565. []
  38. GOAT is essential for ghrelin-mediated elevation of GH, necessary to prevent death from severe calorie restriction through preservation of blood glucose levels. []
  39. Ghrelin O-acyltransferase (GOAT) is essential for growth hormone-mediated survival of calorie-restricted mice. Zhao TJ, Liang G, Li RL, Xie X, Sleeman MW, Murphy AJ, Valenzuela DM, Yancopoulos GD, Goldstein JL, Brown MS. Proc Natl Acad Sci U S A. 2010 Apr 20; 107(16):7467-72. []
  40. Positive Feedback – a physiological cyclic process or action that can continue to amplify the body’s response to a stimulus until a negative feedback response, its opposite, takes over. []
  41. AgRP neurons – brain neurons that make agouti-related peptides – hence AgRP – that potently stimulate food intake []
  42. Hunger Circuit. Science Signalling. by W Wong – ‎2011. []
  43. Intestinal mobility is the movements of the digestive system, and the transit of the contents within it. []
  44. A secretagogue is a substance that stimulates secretion of another substance – in this case, ghrelin stimulates the release of growth factor (GH) from the pituitary gland. []
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  47. A neoplasm is an abnormal new growth of cells. The cells in a neoplasm usually grow more rapidly than normal cells and will continue to grow if not treated. []
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  49. Wiley Online Library: Obese children aged 4–6 displayed decreased fasting and postprandial ghrelin levels in response to a test meal. Jenny Önnerfält, Charlotte Erlanson‐Albertsson, Caroline Montelius, Kristina Thorngren‐Jerneck. 24 November 2017. []
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  60. Downregulation is the process of reducing or suppressing a response to a stimulus. In this case, it’s a reduction in a cellular responses to ghrelin molecules due to changes in the number of activity of receptors. []
  61. Growth hormone is released from the pituitary gland to cause growth in children and affects bone density, lipid metabolism, and muscle in children and adults, stimulating amino acid uptake and protein synthesis in muscle and other tissues. Because a major role of growth hormone is to to stimulate the liver and other tissues to secrete IGF-1, this can be a problem if too much IGF-1 is produced in adults. Due to its insulin-like properties, IGF-1 can have serious and potentially fatal health effects including: diabetic (hypoglycaemic) coma, heart palpitations (tachycardia), facial nerve pain or paralysis (Bells Palsy), swelling of the hands, and so forth. []
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  63. Hypoadiponectinaemia is characterised by low plasma adiponectin levels – 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. []
  64. Hyperleptinaemia is the presence of a higher than normal amount of leptin in the bloodstream. []
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  66. Lipolysis is the breakdown of lipids and involves hydrolysis of triglycerides into glycerol and free fatty acids. It mainly occurs in adipose tissue, and is used to mobilise stored energy during fasting or exercise. []
  67. Truncal adiposity refers to obesity – fat retention – around the trunk of the body. []
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  69. Positive energy balance occurs when the intake of food is greater than the output of work (as in muscular or secretory activity). The result is that the body stores extra food as fats. Negative energy balance occurs when the body draws on stored fat to provide energy for work. []
  70. Anabolism is a process a process that involves the synthesis of complex molecules from simpler molecules. These processes produce growth and differentiation of cells and increases in body size. Examples of anabolic processes include the growth and mineralisation of bone and increases in muscle mass. []
  71. Catabolism is the set of metabolic pathways that breaks down molecules into smaller units that are either oxidised to release energy or used in other anabolic reactions. []
  72. Negative energy balance is when energy demands exceed caloric supply – the opposite of positive energy balance. []
  73. A.A. Sakharova, J.F. Horowitz, S. Surya, N. Goldenberg, M.P. Harber, K. Symons, A. Barkan, Role of growth hormone in regulating lipolysis, proteolysis, and hepatic glucose production during fasting. J. Clin. Endocrinol. Metab. 93, 2755–2759. 2008. []
  74. Endocrine. June 2015, Volume 49, Issue 2, pp 304–306. Growth hormone deficiency in patients with obesity. Roberto Salvatori. []
  75. Ghrelin and growth hormone: Story in reverse. Ralf M. Nass, Bruce D. Gaylinn, Alan D. Rogol, and Michael O. Thorner. PNAS May 11, 2010 107 (19) 8501-8502. []
  76. Cummings DE, Weigle DS, Frayo RS, Breen PA, Ma MK, Dellinger EP, Purnell JQ. Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med. 2002;346(21):1623–1630. []
  77. Geloneze B, Tambascia MA, Pilla VF, Geloneze SR, Repetto EM, Pareja JC. Ghrelin: a gut-brain hormone: effect of gastric bypass surgery. Obes Surg. 2003;13(1):17–22. []
  78. Can The UK Government Really Combat Child Obesity? []
  79. England’s Obesity Hotspots []
  80. Vegan Pregnancy & Parenting []
  81. Bliss Points, Pleasure Traps & Wholefood Plant-Based Diets []
  82. Malabsorption occurs when the small intestine can’t absorb enough of certain nutrients and fluids – including macronutrients – proteins, carbohydrates, and fats – and micronutrients – vitamins and minerals – or both []
  83. relating to the body fluids, especially with regard to immune responses involving antibodies in body fluids as distinct from cells []
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  85. Roux-en-y gastric bypass (RYGB) – from César Roux, the surgeon who first described it – a form of anastomosis – an anastomosis is a connection or opening between two things that are normally diverging or branching, such as between blood vessels, leaf veins, or streams – involving a division of the small intestine, resulting in a Y-shaped configuration []
  86. Sleeve Gastrectomy (SG) – a surgical weight-loss procedure in which the stomach is reduced to about 15% of its original size, by surgical removal of a large portion of the stomach along the greater curvature. []
  87. Liou JM, Lin JT, Lee WJ, Wang HP, Lee YC, Chiu HM, Wu MS. The serial changes of ghrelin and leptin levels and their relations to weight loss after laparoscopic minigastric bypass surgery. Obes Surg. 2008;18(1):84–89. []
  88. The distal small intestine is the part furthest from the stomach – the ileum. []
  89. Morbid Obesity Solution: A Long-Term Plant-Based Case Study. 24 Jan 2017. []
  90. ResearchGate. Serum ghrelin level is associated with cardiovascular risk score. Romanian journal of internal medicine. 53(2):140-5 · September 2015. []
  91. Aging Cell. 2017 Aug;16(4):859-869. doi: 10.1111/acel.12618. Epub 2017 Jun 6. Deletion of ghrelin prevents aging-associated obesity and muscle dysfunction without affecting longevity. Guillory B1, Chen JA, Patel S, Luo J, Splenser A, Mody A, Ding M, Baghaie S, Anderson B, Iankova B, Halder T, Hernandez Y, Garcia JM. []
  92. Aging Cell. 2017 Aug; 16(4): 859–869. Deletion of ghrelin prevents aging‐associated obesity and muscle dysfunction without affecting longevity. Bobby Guillory et al. []
  93. Korek E, Krauss H, Gibas-Dorna M, Kupsz J, Piatek M, Piatek J. Fasting and postprandial levels of ghrelin, leptin and insulin in lean, obese and anorexic subjects. Prz Gastroenterol. 2013;8(6):383–389. []
  94. Mequinion M, Langlet F, Zgheib S, Dickson S, Dehouck B, Chauveau C, Viltart O. Ghrelin: central and peripheral implications in anorexia nervosa. Front Endocrinol (Lausanne) 2013;4:15. []
  95. Bulimia nervosa is an emotional disorder characterised by a distorted body image and an obsessive desire to lose weight, in which bouts of extreme overeating are followed by fasting or self-induced vomiting or purging. []
  96. Pathophysiology or physiopathology is the disordered physiological processes associated with disease or injury. []
  97. ResearchGate. Getting to the bottom of feeding behaviour: Who’s on top? Applied Physiology Nutrition and Metabolism 32(2):177-89 · May 2007. []
  98. Psychoneuroendocrinology. 2013 Mar. Dysfunctions of leptin, ghrelin, BDNF and endocannabinoids in eating disorders: beyond the homeostatic control of food intake. Monteleone P, Maj M. []
  99. Cell Metabolism. Volume 27, issue 1, P42-56, January 09, 2018. Overlapping Brain Circuits for Homeostatic and Hedonic Feeding. Mark A. Rossi, Garret D. Stuber. []
  100. Cheung CK, Wu JC. Role of ghrelin in the pathophysiology of gastrointestinal disease. Gut Liver. 2013;7(5):505–512. [] []
  101. Intra-peritoneal means within or administered through the peritoneum – the thin, transparent membrane that lines the walls of the abdominal (peritoneal) cavity and contains/encloses the abdominal organs such as the stomach and intestines []
  102. systemic administration is a route of administration of medication, nutrition or other substance into the circulatory system so that the entire body is affected. Administration can take place via either, 1. enteral, that is, via the gastrointestinal tract by oral, sublingual, oesophagus, stomach, small/large intestine and rectum, or by 2. parenteral administration, that is via means that bypass the gastrointestinal tract, mainly by intramuscular, subcutaneous, or intravenous injections that bypass skin and mucous membranes []
  103. Morphology is a branch of biology dealing with the study of the form and structure of organisms and their specific structural features. []
  104. The Ghrelin Axis—Does It Have an Appetite for Cancer Progression? Lisa K. Chopin Inge Seim Carina M. Walpole Adrian C. Herington. Endocrine Reviews, Volume 33, Issue 6, 1 December 2012, Pages 849–891. []
  105. radioimmunoassay is a technique for determining antibody levels by introducing an antigen (a toxin or other foreign substance which induces an immune response in the body, especially the production of antibodies) labelled with a radioisotope and measuring the subsequent radioactivity of the antibody component []
  106. Feigerlová E, Diene G, Conte-Auriol F, et al. Hyperghrelinemia precedes obesity in Prader-Willi syndrome. J Clin Endocrinol Metab 2008;93:2800-5. 10.1210/jc.2007-2138 []
  107. Gumus Balikcioglu P, Balikcioglu M, Muehlbauer MJ, et al. Macronutrient Regulation of Ghrelin and Peptide YY in Pediatric Obesity and Prader-Willi Syndrome. J Clin Endocrinol Metab 2015;100:3822-31. 10.1210/jc.2015-2503 []
  108. Am J Med Genet A. 2015 Jan;167A(1):69-79. doi: 10.1002/ajmg.a.36810. Epub 2014 Oct 29. Hyperghrelinemia in Prader-Willi syndrome begins in early infancy long before the onset of hyperphagia. Kweh FA, Miller JL, Sulsona CR, Wasserfall C, Atkinson M, Shuster JJ, Goldstone AP, Driscoll DJ. []
  109. Hyperghrelinaemia is, as the name suggests, an abnormally high level of ghrelin. []
  110. Transl Pediatr. 2017 Oct; 6(4): 274–285. Review of Prader-Willi syndrome: the endocrine approach. Ryan Heksch, Manmohan Kamboj, Kathryn Anglin,Kathryn Obrynba. []
  111. Surviving Starvation: The Ghrelin-Growth Hormone Axis. Part 1. []
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  113. PYY (Peptide YY or peptide tyrosine tyrosine)  – a peptide that in humans is encoded by the PYY gene. Peptide YY is a short peptide released from cells in the ileum and colon. Soon after eating, and before food reaches the lower small intestine (ileum), PYY is secreted into the blood by cells lining the ileum and colon. []
  114. Nature. 2002 Aug 8;418(6898):650-4. Gut hormone PYY(3-36) physiologically inhibits food intake. Batterham RL, Cowley MA, Small CJ, Herzog H, Cohen MA, Dakin CL, Wren AM, Brynes AE, Low MJ, Ghatei MA, Cone RD, Bloom SR. []
  115. Braz J Med Biol Res. 2012 Jul; 45(7): 656–664. Correlations of circulating peptide YY and ghrelin with body weight, rate of weight gain, and time required to achieve the recommended daily intake in preterm infants. XiaFang Chen et al. []
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  118. CNS. Morbid Obesity Solution: A Long-Term Plant-Based Case Study. By Roberta Russell. January 24, 2017. []
  119. Obesity. []
  120. Toxic Hunger vs Real Hunger []

Leptin – The “Fat” Hormone?

If you’re not familiar with leptin, it’s certainly familiar with you. Known by various nicknames, such as the ‘satiety hormone’ or ‘fat hormone’, leptin plays a leading role in daily dietary dramas. But, is it more responsible for over-eating (hyperphagia) and obesity than mere lack of will-power?

What is leptin?

In healthy, non-obese individuals, the hormone leptin controls appetite. After you’ve eaten a meal, this anorexigenic (appetite-suppressing) hormone gets released by adipose tissue (fat cells) and acts on the hypothalamus in the brain to produce a feeling of satiety (fullness) which then suppresses the appetite and (hopefully) stops you from over-eating. It also speeds up your resting metabolism, thereby increasing energy expenditure. 1

This is a pretty sensible mechanism, from an evolutionary point of view, since it would help stop members of our species from getting too fat to be able to run away from sabre-toothed tigers. 2

On the other hand, there were perfectly good reasons why we might have needed to store up as much fat as possible –  to get through periods of famine, for instance. 3 This is why there are mechanisms, including the orexigenic (appetite-stimulating) hormone ghrelin (the “hunger hormone“) 4 , which act in the opposite direction from leptin, actively stimulating us to feel hungry5

However, evolution wasn’t so good at predicting the appearance of McDonald’s Whoppers or Chocolate Hobnobs. And this is where the problem starts with leptin. If we continue to eat the ‘wrong’ foods, the brain doesn’t realise we’ve actually had enough to eat.

Before looking into a bit more detail about why leptin might not be doing its job properly – evident by the widespread increase in obesity – it’s worth mentioning that other mechanism supposed to help us moderate food intake – namely, stretch receptors in the stomach 6 . If these are supposed to activate as the stomach expands in size, you can see from the above graphic that high-calorie/low-bulk foods will not stretch the stomach as much as low-calorie/high-bulk foods – that is, plant foods which are high in fibre content.

Such foods (mostly processed with high levels of sugar, saturated fat and salt) tend to be high in calories but low in nutrients (such as fibre, vitamins, minerals and phytonutrients). 7 . This is where we come across the differences between toxic hunger and real hunger, as discussed in a previous blog 8 . It’s called “toxic” because it can end up causing us to chronically over-eat and become obese, resulting in all the nasty associated problems like type 2 diabetes, heart disease and various cancers.

Leptin – Animal-Eaters vs Plant-Eaters

So, turning back to leptin, a recent study 9 took a small number of healthy women from three different dietary groups: omnivores, lacto-ovo-vegetarians, and vegans to see if there were any difference in leptin levels between them. What they found was in line with previous studies 10 11 12 , namely: “…people who adopted a vegetarian dietary pattern had lower plasma levels of leptin when compared to the meat consumers.” The mean plasma leptin levels were:

  • omnivores – 7.45 ng/ml
  • lacto-ovo-vegetarians – 3.87 ng/ml
  • vegans – 2.89 ng/ml

Leptin & Obesity

It’s well-established that meat-eaters are more likely than plant-eaters to become obese 13 14 . So, does this mean that meat-eaters don’t have enough leptin to inform their brains that they have eaten enough, and that plant-eaters have too much leptin? Oddly enough, quite the reverse.

Leptin Insensitivity/Resistance

What’s actually happening is that the abundance of swollen fat cells produce so much leptin that the hypothalamus starts to become insensitive and eventually resistant to leptin’s action. Thus, the brain keeps telling the obese individual “You’re still hungry!“. Eating plant-based diets – ideally WFPB diets, since vegan diets can still lead to obesity if they contain loads of junk food 15 – does not result in such fat storage in the body and, hence, leptin continues to do its job without the body getting “fed up of it”…

You’ve probably already drawn a parallel here with leptin resistance/insensitivity – namely, to type 2 diabetes. By definition, T2D is a condition which transitions through a stage where the pancreas still pumps plenty of insulin into the bloodstream, but cells become resistant/insensitive to it 16 .

It’s similar to how taste buds become insensitive to salt and sugar, how one can develop tolerance for cigarettes or alcohol, even though the body is silently screaming.

Do I Need To Increase Leptin levels?

Perhaps the more appropriate question should be “How do I make my body more sensitive to the already high levels of leptin in my body?”

The simplest and healthiest way is likely to be through changing to a plant-based diet. Not only is this likely to clear up any existing problem with leptin resistance, it will also help to reverse a huge range of diseases – including obesity 17 , type 2 diabetes 18 , cardiovascular disease 19 , and even many cancers 20 .

Final thoughts

The above brief analysis has suggested that, A. leptin works best within non-obese bodies and, B. that non-obese bodies are more likely to be inhabited by plant-eaters than by meat-eaters.

We also know that plant-eaters are less likely than omnivores to suffer from metabolic syndrome –  a complex of conditions in which triglycerides, total cholesterol, low-density lipoprotein (LDL), blood glucose, blood pressure, waist circumference, and body mass index (BMI) are all increased to seriously unhealthy levels21 .

It’s The Fat!

And much of the problem is simply to do with the amount of fat within the body – not that we grow more fat cells, since we actually retain a reasonably constant number of fat cells throughout adult life 22 , rather the fat cells we have can grow and grow until they’re so stuffed full that they leach fat back into the bloodstream without us even needing to consume any dietary fat –  a process known as “reintoxication” 23 Yuk!

So What About Will-Power?

It’s so easy to think that overweight/obese individuals lack sufficient will-power. However, it may be more likely that they are simply acting in accordance with what their brain is telling them or, rather, what their brain is failing to tell them.

How Do I Know If I’m Leptin Resistant?

It may sound too simple, but – just look in the mirror or see if you can grab a handful of fat around the middle of your body. Basically, there’s a really strong chance that leptin is not doing its job inside you if you are overweight.

How Do I Reverse Leptin Resistance?

I keep hammering away at this…but, all the evidence strongly suggests that the healthiest, most natural and sustainable diet for weight loss, general disease-resistance and healthy longevity is a wholefood plant-based diet24 25 . It’s also probably the healthiest for the rest of life on Earth, too 26 .

How about having a go at the short quiz below?

[qsm quiz=18]


  1. Waugh, Anne; Grant, Allison. Ross & Wilson Anatomy and Physiology in Health and Illness E-Book (p. 284). Elsevier Health Sciences. Kindle Edition. []
  2. The evolution of body fatness: trading off disease and predation risk. John R. Speakman. []
  3. A Nonadaptive Scenario Explaining the Genetic Predisposition to Obesity: The “Predation Release” Hypothesis. Literature Review. Cell Metabolism 6(1):5-12 · August 2007. []
  4. Ghrelin is the primary hunger hormone. It’s released from your stomach (with smaller amounts being released by the small intestine, pancreas and brain) into the blood and to the brain to stimulate hunger to alert you that you’re hungry. It has many functions throughout your body besides hunger. It also functions within the pleasure/reward centre of the brain, and plays a role in memory formation, immune function, and even sleep. []
  5. Curr Opin Clin Nutr Metab Care. 2013 Nov; 16(6): 619–624. Ghrelin: much more than a hunger hormone. Geetali Pradhan, Susan L. Samson, and Yuxiang Sun. []
  6. Paintal, A. S. (1954). A study of gastric stretch receptors. Their role in the peripheral mechanism of satiation of hunger and thirst. The Journal of Physiology, 126(2), 255–270. []
  7. Health = Nutrient Intake ÷ Calories []
  8. Toxic Hunger vs Real Hunger []
  9. Association between different types of plant-based diets and leptin levels in healthy volunteers. Gogga P, Śliwińska A, Aleksandrowicz-Wrona E, Małgorzewicz S. Acta Biochim Pol. 2019 Feb 15. doi: 10.18388/abp.2018_2725. []
  10. AmbroszkiewiczJ,Laskowska-Klita T,Klemarczyk W (2004) Low se-rum leptin concentration in vegetarian prepubertal children. Rocz Akad Med Bialymst 49: 103–105. []
  11. AmbroszkiewiczJ,Klemarczyk W,Gajewska J,Chełchowska M,Ro-wicka G, Ołtarzewski M, Laskowska-Klita T (2011) Serum concen-tration of adipocytokines in prepubertal vegetarian and omnivorous children. Med Wieku Rozwoj 15: 326–334 []
  12. Kim MH, Bae YJ (2015) Comparative study of serum leptin and insu-lin resistance levels betweenKorean postmenopausalvegetarianandnon-vegetarian women. Clin Nutr Res 4: 175–181. []
  13. Int J Obes (Lond). 2009 Jun; 33(6): 621–628. Meat consumption is associated with obesity and central obesity among US adults. Y Wang and MA Beydoun. []
  14. Vegetarian diets and childhood obesity prevention. Joan Sabaté Michelle Wien. The American Journal of Clinical Nutrition, Volume 91, Issue 5, 1 May 2010, Pages 1525S–1529S. []
  15. Greggs’ Vegan Sausage Rolls – Why Veganism Can Fail []
  16. Every vampire needs an invitation []
  17. CNS: Morbid Obesity Solution: A Long-Term Plant-Based Case Study. Roberta Russell. January 24, 2017. []
  18. J Geriatr Cardiol. 2017 May; 14(5): 342–354. A plant-based diet for the prevention and treatment of type 2 diabetes. Michelle McMacken and Sapana Shah. []
  19. J Geriatr Cardiol. 2017 May; 14(5): 317–320. A plant-based diet and coronary artery disease: a mandate for effective therapy. Caldwell B Esselstyn. []
  20. Surely Foods Can’t Fight Cancer []
  21. RizzoNS,Sabaté J,Jaceldo-Siegl K,Fraser GE (2011) Vegetariandietary patterns are associated with a lower risk of metabolic syn-drome: the adventist health study 2. Diabetes Care 34: 1225–1227. []
  22. NIH RESEARCH MATTERS. May 12, 2008. Fat Cell Numbers in Teen Years Linger for a Lifetime. []
  23. Br J Pharmacol. 2009 Nov; 158(5): 1330–1337. Reintoxication: the release of fat-stored Δ9-tetrahydrocannabinol (THC) into blood is enhanced by food deprivation or ACTH exposure. N Gunasekaran et al. []
  24. Which Diets Work for Weight-Loss? []
  25. Vegetarian Diets and the Risk of Diabetes []
  26. A Sustainable Diet for Our Planet []

The Importance of Sleep

One of my clients emailed me to say that he was concerned about his blood pressure. On the WFPB programme for nearly four weeks, his blood pressure has been dropping consistently from around 160/100 when he started, to 113/78 two days ago. Then it looked like it was starting to rise again. I sensed some panic in his tone…

When I looked at his nutritional/lifestyle diary for the past days I could see the problem – sleep or rather the lack of it.

A recent study of US citizens found that 1 in 3 were chronically sleep deprived. It is likely figures for other Western countries are similar. Sleep – or, rather, the lack of it – is a BIG problem for many people.

Health conditions associated with lack of sleep

And what few fully appreciate is that blood pressure (BP) rises if you have insufficient sleep. And raised BP is not all. The following are also associated with sleep deficiency:

Suggestions for improving quality of sleep

So, how do we ensure that we stand the best chance of getting enough good quality sleep? The following are associated with improved sleep patterns according to both third-party studies and my own professional/personal experience:

A little more detail…

More on the benefits of plant-based diets

More advice on optimal amounts of sleep.

More on sleep and the immune system.

More on the relationship between cherries, kiwifruit and sleep.

A note about melatonin

Melatonin is a hormone secreted at night by the pineal gland in the center of our brain to help regulate our circadian rhythm. Supplements are used to prevent and reduce jet lag. MIT got the patent to use melatonin to help people sleep. But melatonin “is not only produced in the pineal gland—it is also naturally present in edible plants.

For more information on melatonin.

The above is by no means meant to be a comprehensive list of the chronic health conditions associated with sleep deficiency; nor have I provided a definitive list of suggestions for improving sleep quality. If it forms a basis for discussion or for you to undertake your own research (and send me the findings, please!) then that is a sufficient achievement.

What I will add is that the four cornerstones of health that I continue to mention (diet, sleep, exercise and stress-avoidance) are all a part of the wholistic approach that I consider optimal for human health and well-being.

Diet is perhaps the most important element in all of this, since it forms the basis for being able to sleep well, recover from and endure exercise, and enjoy a positive, stress-reduced mental attitude. Part of the reason why it is able to do this is because it is fundamental to maintaining the body in a state of homeostasis (balance), rather than having to constantly detoxify, protect and repair itself from the inferior “foods” we have so often forced our poor bodies to eat.

Wholistic = Diet+Exercise+Sleep+Stress Reduction…They work together. They compliment one another.

A few final words from Dr Neal Barnard about high-protein foods and sleep

“While many people believe that high-protein meals are key to getting a good night’s rest, the opposite is true. High-protein foods block the brain’s ability to produce serotonin. Because high-protein foods contain more amino acids, tryptophan—the amino acid that eventually turns into serotonin—is crowded out of the brain. As a result, high-protein foods will leave you feeling alert.

High-protein plant-based foods, like tofu, beans, and lentils, are very nutritious. But if you’re having trouble sleeping, try eating these foods earlier in the day. You’ll feel more alert during the day, while favoring carbohydrates later on can help you rest at night.”

Dr Neal Barnard in his own words:


Health conditions associated with lack of sleep (in addition to the above links)

Osamu Tochikubo, Akihiko Ikeda, Eiji Miyajima, Masao Ishii. Hypertension. 1996;27:1318-1324.
Originally published June 1, 1996. Effects of Insufficient Sleep on Blood Pressure Monitored by a New Multibiomedical Recorder.

Noguti J, Andersen ML, Cirelli C, Ribeiro DA. Sleep Breath. 2013 Sep;17(3):905-10. doi: 10.1007/s11325-012-0797-9. Epub 2013 Feb 1. Oxidative stress, cancer, and sleep deprivation: is there a logical link in this association?

Redeker NS, Pigeon WR, Boudreau EA. Support Care Cancer. 2015 Apr;23(4):1145-55. doi: 10.1007/s00520-014-2537-0. Epub 2014 Dec 16.
Incorporating measures of sleep quality into cancer studies.

Wang P, Ren FM, Lin Y, Su FX, Jia WH, Su XF, Tang LY, Ren ZF. Sleep Med. 2015 Apr;16(4):462-8. doi: 10.1016/j.sleep.2014.11.017. Epub 2015 Feb 3. Night-shift work, sleep duration, daytime napping, and breast cancer risk.

Olsson M, Ärlig J, Hedner J, Blennow K1, Zetterberg H. Sleep. 2018 Feb 7. doi: 10.1093/sleep/zsy025. Sleep Deprivation and CSF Biomarkers for Alzheimer Disease.

Ju YE, McLeland JS, Toedebusch CD, Xiong C, Fagan AM, Duntley SP, Morris JC, Holtzman DM. AMA Neurol. 2013 May;70(5):587-93. doi: 10.1001/jamaneurol.2013.2334. Sleep quality and preclinical Alzheimer disease.

Malhotra RK. Sleep Med Clin. 2018 Mar;13(1):63-70. doi: 10.1016/j.jsmc.2017.09.006. Epub 2017 Nov 10. Neurodegenerative Disorders and Sleep.

Holingue C, Wennberg A, Berger S, Polotsky VY, Spira AP. Metabolism. 2018 Jan 31. pii: S0026-0495(18)30029-5. doi: 10.1016/j.metabol.2018.01.021. Disturbed Sleep and Diabetes: A Potential Nexus of Dementia Risk.

Lao XQ, Liu X, Deng HB, Chan TC, Ho KF, Wang F, Vermeulen R, Tam T, Wong MCS, Tse LA, Chang LY, Yeoh EK. J Clin Sleep Med. 2018 Jan 15;14(1):109-117. doi: 10.5664/jcsm.6894. Sleep Quality, Sleep Duration, and the Risk of Coronary Heart Disease: A Prospective Cohort Study With 60,586 Adults.

Solarz DE, Mullington JM, Meier-Ewert HK. Front Biosci (Elite Ed). 2012 Jun 1;4:2490-501. Sleep, inflammation and cardiovascular disease.

Ancoli-Israel S, DuHamel ER, Stepnowsky C, Engler R, Cohen-Zion M, Marler M. Chest. 2003 Oct;124(4):1400-5. The relationship between congestive heart failure, sleep apnea, and mortality in older men.

Fletcher EC. Monaldi Arch Chest Dis. 1996 Feb;51(1):77-80. Obstructive sleep apnoea and cardiovascular morbidity.

Patyar S, Patyar RR.. J Stroke Cerebrovasc Dis. 2015 May;24(5):905-11. doi: 10.1016/j.jstrokecerebrovasdis.2014.12.038. Epub 2015 Mar 25. Correlation between Sleep Duration and Risk of Stroke.

Miller MA, Kruisbrink M, Wallace J, Ji C, Cappuccio FP. Sleep. 2018 Feb 1. doi: 10.1093/sleep/zsy018. Sleep Duration and Incidence of Obesity in Infants, Children and Adolescents: A Systematic Review and Meta-Analysis of Prospective Studies.

Bell JF, Zimmerman FJ. Arch Pediatr Adolesc Med. 2010 Sep;164(9):840-5. doi: 10.1001/archpediatrics.2010.143. Shortened nighttime sleep duration in early life and subsequent childhood obesity.

Hart CN, Jelalian E. Behav Sleep Med. 2008;6(4):251-67. doi: 10.1080/15402000802371379. Shortened sleep duration is associated with pediatric overweight.

Taveras EM, Gilliman MW, Pena MM, Redline S, Rifas Shiman SL. Jun;133(6):1013-22. Pediatrics. 2014. Chronic Sleep Curtailment and Adiposity.

Patel SR, Hu FB. Obesity (Silver Spring). 2008; 16:643-53. Short sleep duration and weight gain: a systematic review.

PatelSR, Malhotra A, White DP, Gottlieb DJ, Hu FB. Am J Epidemiol.2006; 164:947-54. Association between reduced sleep and weight gain in women.

Kim CW, Chang Y, Sung E, Ryu S.. Diabet Med. 2017 Nov;34(11):1591-1598. doi: 10.1111/dme.13432. Epub 2017 Aug 14. Sleep duration and progression to diabetes in people with prediabetes defined by HbA1c concentration.

Briançon-Marjollet A, Weiszenstein M, Henri M, Thomas A, Godin-Ribuot D, Polak J. Diabetol Metab Syndr. 2015 Mar 24;7:25. doi: 10.1186/s13098-015-0018-3. eCollection 2015. The impact of sleep disorders on glucose metabolism: endocrine and molecular mechanisms.

Orzeł-Gryglewska J. Int J Occup Med Environ Health. 2010;23(1):95-114. doi: 10.2478/v10001-010-0004-9. Consequences of sleep deprivation. [Immunological changes]

Riemann D, Baglioni C, Spiegelhalder K. Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz. 2011 Dec;54(12):1296-302. doi: 10.1007/s00103-011-1378-y. [Lack of sleep and insomnia. Impact on somatic and mental health]. [Article in German]

Riemann D. Sleep Med. 2007 Dec;8 Suppl 4:S15-20. doi: 10.1016/S1389-9457(08)70004-2. Insomnia and comorbid psychiatric disorders.

Papadimitriou GN, Linkowski P. Int Rev Psychiatry. 2005 Aug;17(4):229-36. Sleep disturbance in anxiety disorders.

Roehrs T, Hyde M, Blaisdell B, Greenwald M, Roth T. Sleep. 2006 Feb;29(2):145-51. Sleep loss and REM sleep loss are hyperalgesic. [Increased cute/chronic pain sensitivity]

Alexandre C, Latremoliere A, Ferreira A, Miracca G, Yamamoto M, Scammell TE, Woolf CJ. Nat Med. 2017 Jun;23(6):768-774. doi: 10.1038/nm.4329. Epub 2017 May 8. Decreased alertness due to sleep loss increases pain sensitivity in mice.

Oyetakin-White P, Suggs A, Koo B, Matsui MS, Yarosh D, Cooper KD, Baron ED. Clin Exp Dermatol. 2015 Jan;40(1):17-22. doi: 10.1111/ced.12455. Epub 2014 Sep 30. Does poor sleep quality affect skin ageing?

Pastuszak AW, Moon YM, Scovell J, Badal J, Lamb DJ, Link RE, Lipshultz LI. Urology. 2017 Apr;102:121-125. doi: 10.1016/j.urology.2016.11.033. Epub 2016 Dec 14. Poor Sleep Quality Predicts Hypogonadal Symptoms and Sexual Dysfunction in Male Nonstandard Shift Workers.

Hirotsu C, Soterio-Pires JH, Tufik S, Andersen ML. Int J Impot Res. 2017 May;29(3):126. doi: 10.1038/ijir.2017.1. Epub 2017 Feb 16. Sleep disturbance and sexual dysfunction in postmenopausal women.

Opstad PK.. J Clin Endocrinol Metab. 1992 May;74(5):1176-83. Androgenic hormones during prolonged physical stress, sleep, and energy deficiency. 9 [Adrenal & Testicular Androgens]

Sheldon Cohen, PhD, William J. Doyle, PhD, Cuneyt M. Alper, MD, Denise Janicki-Deverts, PhD, and Ronald B. Turner, MD. Arch Intern Med. Author manuscript; available in PMC 2010 Jan 12. Published in final edited form as:Arch Intern Med. 2009 Jan 12; 169(1): 62–67.
doi: 10.1001/archinternmed.2008.505. Sleep Habits and Susceptibility to the Common Cold.

Liu TZ, Xu C, Rota M, Cai H, Zhang C, Shi MJ, Yuan RX, Weng H, Meng XY, Kwong JS, Sun X. Sleep Med Rev. 2017 Apr;32:28-36. doi: 10.1016/j.smrv.2016.02.005. Epub 2016 Mar 3. Sleep duration and risk of all-cause mortality: A flexible, non-linear, meta-regression of 40 prospective cohort studies.

Tso W, Rao N, Jiang F, Li AM, Lee SL, Ho FK, Li SL, Ip P. J Pediatr. 2016 Feb;169:266-71. doi: 10.1016/j.jpeds.2015.10.064. Epub 2015 Nov 19. Sleep Duration and School Readiness of Chinese Preschool Children.

Street NW, McCormick MC, Austin SB, Slopen N4 Habre R, Molnar BE. Sleep Health. 2016 Jun;2(2):129-135. doi: 10.1016/j.sleh.2016.03.002. Epub 2016 Apr 18. Sleep duration and risk of physical aggression against peers in urban youth.

Luyster FS, Strollo PJ Jr, Zee PC, Walsh JK; Boards of Directors of the American Academy of Sleep Medicine and the Sleep Research Society. Sleep. 2012 Jun 1;35(6):727-34. doi: 10.5665/sleep.1846. Sleep: a health imperative. [Increased risk of fatal accidents]

Philip P, Akerstedt T. Sleep Med Rev. 2006 Oct;10(5):347-56. Epub 2006 Aug 22. Transport and industrial safety, how are they affected by sleepiness and sleep restriction?

Akerstedt T, Kecklund G, Alfredsson L, Selen J. J Sleep Res. 2007 Dec;16(4):341-5. Predicting long-term sickness absence from sleep and fatigue.

Lim J, Dinges DF. Psychol Bull. 2010 May;136(3):375-89. doi: 10.1037/a0018883. A meta-analysis of the impact of short-term sleep deprivation on cognitive variables.

Esposito MJ, Occhionero M1, Cicogna P. Sleep. 2015 Nov 1;38(11):1823-6. doi: 10.5665/sleep.5172. Sleep Deprivation and Time-Based Prospective Memory.

Lima AM, de Bruin VM, Rios ER, de Bruin PF. Naunyn Schmiedebergs Arch Pharmacol. 2014 May;387(5):399-406. doi: 10.1007/s00210-013-0955-z. Epub 2014 Jan 15. Differential effects of paradoxical sleep deprivation on memory and oxidative stress.

Eun Yeon Joo, Cindy W Yoon, Dae Lim Koo, Daeyoung Kim and Seung Bong Hong/ J Clin Neurol. 2012 Jun;8(2):146-150. English.
Published online June 29, 2012. Adverse Effects of 24 Hours of Sleep Deprivation on Cognition and Stress Hormones.


Suggestions for improving quality of sleep (in addition to the above links)

Nutr Res. 2012 May;32(5):309-19. doi: 10.1016/j.nutres.2012.03.009. Epub 2012 Apr 25. Peuhkuri K, Sihvola N, Korpela R. Diet promotes sleep duration and quality.

St-Onge MP, Roberts A, Shechter A, Choudhury AR. J Clin Sleep Med. 2016 Jan;12(1):19-24. doi: 10.5664/jcsm.5384. Fiber and Saturated Fat Are Associated with Sleep Arousals and Slow Wave Sleep.

G. Howatson, P. G. Bell, J. Tallent, B. Middleton, M. P. McHugh, J. Ellis. Eur J Nutr 2012 51(8):909 – 916. Effect of tart cherry juice (Prunus cerasus) on melatonin levels and enhanced sleep quality.

H.-H. Lin, P.-S. Tsai, S.-C. Fang, J.-F. Liu. Asia Pac J Clin Nutr 2011 20(2):169 – 174. Effect of kiwifruit consumption on sleep quality in adults with sleep problems.

Brand S, Gerber M, Beck J, Hatzinger M, Pühse U, Holsboer-Trachsler E. J Adolesc Health. 2010 Feb;46(2):133-41. doi: 10.1016/j.jadohealth.2009.06.018. Epub 2009 Aug 18. High exercise levels are related to favorable sleep patterns and psychological functioning in adolescents: a comparison of athletes and controls.

Thakkar MM, Sharma R, Sahota P. Alcohol. 2015 Jun;49(4):299-310. doi: 10.1016/j.alcohol.2014.07.019. Epub 2014 Nov 11. Alcohol disrupts sleep homeostasis.

Ebrahim IO, Shapiro CM, Williams AJ, Fenwick PB. Alcohol Clin Exp Res. 2013 Apr;37(4):539-49. doi: 10.1111/acer.12006. Epub 2013 Jan 24. Review. Alcohol and sleep I: effects on normal sleep.

Jeanne F. Duffy, M.B.A., Ph.D.a, and Charles A. Czeisler, Ph.D., M.D. Sleep Med Clin. Author manuscript; available in PMC 2010 Jun 1.
Published in final edited form as: Sleep Med Clin. 2009 Jun; 4(2): 165–177. doi: 10.1016/j.jsmc.2009.01.004. Effect of Light on Human Circadian Physiology

Giménez MC, Geerdinck LM, Versteylen M, Leffers P, Meekes GJ, Herremans H, de Ruyter B, Bikker JW, Kuijpers PM, Schlangen LJ. J Sleep Res. 2017 Apr;26(2):236-246. doi: 10.1111/jsr.12470. Epub 2016 Nov 10. Patient room lighting influences on sleep, appraisal and mood in hospitalized people.

Yamauchi M, Jacono FJ, Fujita Y, Kumamoto M, Yoshikawa M, Campanaro CK, Loparo KA, Strohl KP, Kimura H. Sleep Breath. 2014 Dec;18(4):829-35. doi: 10.1007/s11325-014-0951-7. Epub 2014 Feb 13. Effects of environment light during sleep on autonomic functions of heart rate and breathing.

Jones C, Dawson D. Nurs Crit Care. 2012 Sep-Oct;17(5):247-54. doi: 10.1111/j.1478-5153.2012.00501.x. Epub 2012 May 15. Eye masks and earplugs improve patient’s perception of sleep.

Hu RF, Jiang XY, Hegadoren KM, Zhang YH. Crit Care. 2015 Mar 27;19:115. doi: 10.1186/s13054-015-0855-3. Effects of earplugs and eye masks combined with relaxing music on sleep, melatonin and cortisol levels in ICU patients: a randomized controlled trial.

Zaharna M, Guilleminault C. Noise Health. 2010 Apr-Jun;12(47):64-9. doi: 10.4103/1463-1741.63205. Sleep, noise and health: review.

Andrew J.HowellNancy L.DigdonKarenBuro. Personality and Individual Differences (ISSID). Volume 48, Issue 4, March 2010, Pages 419-424. Mindfulness predicts sleep-related self-regulation and well-being.

Huang X, Mazza G. Crit Rev Food Sci Nutr. 2011 Apr;51(4):269-84. doi: 10.1080/10408398.2010.529193. Application of LC and LC-MS to the analysis of melatonin and serotonin in edible plants.

Kehara S, Iso H, Date C, Kikuchi S, Watanabe Y, Wada Y, Inaba Y, Tamakoshi A; JACC Study Group. Association of Sleep Duration with Mortality from Cardiovascular Disease and Other Causes for Japanese Men and Women: the JACC Study. Sleep. 2009 Mar;32(3):295-301.



Wholism vs Reductionism – Not Just a War of Words


You may never have heard of these two terms, “wholism” and “reductionism”, but the war between them is not just a war of words, it’s a war of paradigms. One of these paradigms is unfortunately winning most of the battles, and the result is an escalating public health crisis.

First, let’s look at what I mean by “paradigm”. A good example is the difference between geocentric and heliocentric world views that came to a head around the 15th-16th centuries. Before the so-called Copernican Revolution (involving intellectual giants such as Nicolaus Copernicus (1473-1543), Johannes Kepler (1571-1630) and Galileo Galilei (1564-1642), the accepted and, for the most part, unchallenged paradigm was that the Sun and other planets revolved around the Earth, and the stars were all fixed in the heavens, just like it said in the Bible. Post-Revoltion, there was a slow but ultimately complete “paradigm shift” which meant that everyone now accepts that the Earth and other planets revolve around the Sun, and the stars are no longer just pin-pricks in some form of heavenly firmament.

Put simply, in terms of nutrition, wholism (a term adopted by Professor T Colin Campbell from the similar and better-known term “holism”) deals with whole diet and its effects on the whole person; whereas reductionism looks at specific elements of diet and their effect on specific parts of the person (like a specific gene for loving or hating Marmite).

The seemingly unstoppable increase in diet-related chronic diseases, such as type 2 diabetes and obesity, is simply not being addressed by the ever more precise research being undertaken by scientists, whether they are chemists looking at a specific chemical that can target particular cellular behaviour or a geneticist looking at which gene is responsible for the onset of a particular disease.

Of course it’s necessary to narrow one’s visual field to a specific area of investigation when it is appropriate (for instance, using a microscope to distinguish which virus has infected a given tissue sample); but there is a general tendency nowadays within nutritional science to exclusively apply the microscope (metaphorically speaking) to every public health issue.

Let’s look at an example: A recent report revealed that half of our schoolchildren are now dangerously overweight or obese.

A reductionist response could be to look for and try and isolate the gene that causes obesity in children. £millions or even £billions could be poured into expensive genetic research to find this “needle in the haystack”.  Whereas a wholistic response could be to look at what societal changes have occurred that might account for this unwelcome change in the health of schoolchildren. You don’t have to be a rocket scientist to see that there has been a significant change in the average diets that schoolchildren are now eating when compared to previous generations.

With the reductionist response, one could expect that years and even decades could pass without anything being discovered, and all the while more and more children are likely to become obese.

With the wholistic approach, a solution could theoretically be found very quickly – legislate to improve school meals, increase junk food taxes, ban advertising of unhealthy foods to children, and so forth. The chances are that obesity statistics would start to improve the more practical efforts were made to change laws, educate parents and improve children’s diets. And whilst it might appear that governments do make some moves in this direction, their efforts to implement substantial solutions end up being quasi-wholistic because they are generally hamstrung by the pressure imposed on them by Big Pharma, Big Medicine and Big Agriculture – and the majority of research funding, whether directly or indirectly (e.g. through universities and other institutions), greatly influences which research is most powerfully supported in government circles and reflected in the media to the public.

But even if simple dietary changes could significantly reduce childhood obesity, it would probably not make the reductionists happy. They would still want to delve down into minutiae and find a biological mechanism that could then be controlled somehow, most likely by a drug that could be patented and sold for profit. There is no profit to be made from people simply changing their diets. And there is certainly no profit to be made by pharmaceutical companies or medical organisations from a population full of healthy people.

But let’s say that the geneticists do find a gene that is strongly associated with childhood obesity. It may still take years or decades of research to transfer that information into a fully-tested and certified treatment, probably in the form of a drug.  And even if the obesity pill works in the trials they’ve undertaken, there is no guarantee that it will work within the general population, or that it will be free of serious side-effects only apparent years or decades later (remember Thalidomide?), or if it is too expensive for the majority of people to afford or indeed if the percentage improvement attributable to the drug would bear any comparison with the size of improvement made simply by changing dietary intake.

There is nothing wrong with geneticists exploring the fascinating world of genes, nor is there anything wrong with scientists trying to find what makes one person’s personality different from another’s, or any of the other intriguing questions that beg to be researched and answered by the curious and searching human mind.

What IS a problem, though, is when the ONLY approach to solving scientific problems, particularly those directly linked to public health, is an approach which ignores anything that is “fuzzy” and too…well, human! The funding for most of the scientific research that is undertaken nowadays is only available if there is a tangible and clear hope of achieving a binary, black and white result:

  • 1. A always precedes B.
  • 2. B always follows A.
  • 3. There is no C that could also cause B.

Human behaviour and particularly human nutrition on a population-wide level can never conform to this linear causal pattern. Indeed, even one single cell does not and arguably never can be analysed or understood fully by any amount of analysis – just as can be seen in quantum physics (where electrons can exist in two places at the same time – or cease to exist and reappear elsewhere in ways that can never conform to what we think of as causality), the more we delve into our biochemistry, the more we appreciate how much there is that we can never fully know. Just look at the following diagrammatic representation of just the partial metabolic processes involved in one single cell:

Professor T Colin Campbell explains (1.) the dilemma like this:

“The fact that each nutrient passes through such a maze of reaction pathways suggests that each nutrient also is likely to participate in multiple health and disease outcomes. The one nutrient/one disease relationship implied by reductionism, although widely popular, is simply incorrect. Every nutrient-like chemical that enters this complex system of reactions creates a rippling effect that may extend far into the pool of metabolism. And with every bite of food we eat, there are tens and probably hundreds of thousands of food chemicals entering this metabolism pool more or less simultaneously.”

Whilst it is understandable that the human mind is inquisitive and naturally wants to simplify complexity, is it really essential to map the inter-, intra- and extra-cellular labyrinthine world of the 100 trillion cells comprising the human body before we can identify and apply timely solutions to public health issues?

In any event, our cellular make-up is only one aspect of what constitutes the indefinably complex entity that is a human being. Can we truly ever expect to see a cellular or genetic “cog” that explains what it is to be a friend, a lover, a parent? Why we find beauty in a sunset?

Tackling childhood obesity head-on in the messy “real” world of human populations represents the sort of indeterminate complexity that does not attract large government or institutional funding. More effort goes into producing incomprehensibly complex charts such as the one above than goes into practical measures to help children live full and productive lives. This is not to say that scientists, governments and organisations do not care about the lives of real people – particularly real schoolchildren. Rather, my contention is that they are so wrapped up in doing things the way that things have been done for so long (“stuck inside the paradigm”) that they may, in part, genuinely believe that their way is the ONLY way to solve such public health crises.

This is why I believe it is appropriate to apply the term “paradigm” to the general outlook and approach that science and medicine has been immersed in for at least the past 50 years – probably since the joint effects of two discoveries: the so-called completed list of vitamins and the structure of DNA.  It is also the reason why incredibly convincing population studies, such as The China Study, come under attack from reductionist thinkers. They attack such wide-scale population studies because there is no single causal link demonstrated. This is even the case when the study identifies significant differences in health markers (e.g. cancer, heart disease and type 2 diabetes) between those Chinese populations eating the traditional plant-based diets and those Chinese populations that have adopted the Standard American Diet (SAD).

There is good reason for this lack of indisputable causality: and the reason is that it is simply impossible to prove a single causal link between health and diet when, as Professor Campbell indicated above, no single nutritional input ever causes just one single biochemical response. But such linear responses are just what scientists have habitually expected to discover when the overriding world-view they have been exposed to all their academic and professional lives aims to reduce all complexity down to minute and simple mechanics.

You will have heard the saying “The whole is greater than the sum of its parts”. Intuitively obvious, but possibly not so in the majority of research laboratories around the world.

The assumption that it should be possible to find such a causal link is based on a mechanistic reductionist ideal of the Universe. The likes of Ray Kurtzweil et al consider that one day we will be able to understand everything about ourselves – biology, emotions, personality – by drilling down deeper and deeper, smaller and smaller into the world of micro and nano particles until we find all the little “cogs” and see how they are all connected. We will then be able to predict all events in the “macro world” and reproduce them in better ways with far more durable materials than human flesh and blood.

Of course we don’t want to return to an age of religion and mysticism, where all events were caused by unknown and unknowable forces, spirits and demons. Where everything in biology and personality could be accounted for by the four humours – blood, yellow bile, black bile, and phlegm! We all enjoy huge benefits from the application of reductionist approaches to finding causes and cures for TB and smallpox, and without this approach doctors might still be delivering babies with unwashed hands after having chopped up cadavers or been to the toilet, or both.

Also, I can see how a reductionist approach can be very attractive. It’s neat and orderly and avoids that great enemy of the reductionist thinker, namely, uncertainty.

But I propose that the answer to childhood obesity is both complex and simple.

It’s simple because all it requires is that we feed our children the natural diet for our species (ideally consisting completely or in the main part of whole plant foods), while ensuring that they get some regular exercise.

It’s complex because WE – our biochemistry, our personalities, our societies – ARE complex.

But effective and timely solutions to childhood obesity and many other public health crises are much more likely to be found with the help of two eyes rather than the help of a two million pound electron microscope.

Ample evidence already points to dietary change being the major factor needed in order to solve this escalating health problem. So much evidence, indeed, that I have not even bothered to list it in this article. Just scan through the databases of the NCBI or NIHR to see that sufficient research already links obesity to diet. But in spite of this, the main thrust of government and medical policy derives from what is called “Gold Standard” research, where the majority of research funding (and resultant credibility) is assigned to randomised controlled trials (RCT’s) that control all potential extraneous biases. And, clearly, you cannot do with when dealing with the nutritional and behavioural diversity that exists in the wider world of society as a whole.

This situation can be further explained by the analogy of an elephant in a room along with 60,000 blind scientists who are each responsible for describing one individual facet in minute detail. They can talk at length about the life-cycle of one of the thousands of species of bacteria colonising a crack between two toes, or churn out publications on the chemical components of a particular pigment within a hair from its tail. Yes, it’s true that they become incredibly expert in their own field of research, but it takes just one non-visually impaired child running into the room to be able to announce that there’s a bleedin’ great elephant standing there!

And to the surprise of the child, these 60,000 blind researchers with one voice ask “what’s an elephant?”

To those who have their eyes open to the whole picture, they can see that our example of childhood obesity is but one of the many chronic health conditions clearly caused by diet, and it’s always the same diet, the one that contains far too much animal protein, saturated fats, salt, sugar and processed junk, and far too little whole plant foods.

Diet is a “zero-sum” affair. Whenever one unhealthy food item goes into your mouth it means that another more healthy food item didn’t. And it is the cumulative effect of this, meal after meal, day after day, year after year that leads inexorably to the near-epidemic diet-related health issues that are starting to bring our hospitals to a standstill.

A fish is hooked, thrown onto land, flops around for a bit in the air and then escapes back into the water. Eager to tell his fishy buddies about his experience, he starts talking to them about his time out of the water. “What’s water?” they all ask, looking at him as though he’s out of his scaly mind. When water is all that you know, there is no word for it…

You may enjoy another view of this issue by Dr. Michael Greger…


  1. Campbell, T. Colin. Whole: Rethinking the Science of Nutrition (p. 97). BenBella Books, Inc.. Kindle Edition.


A Fat to Forget


Eating cakes and biscuits appears to impair memory.

Research (1.) suggests that there is relationship between consumption of dietary trans-fats and word-memory.

1018 individuals were given word recall tests that were scored and matched against the amount of trans-fats  consumed by each individual.

The results are worth remembering next time you reach for the cookie jar. Every gram of dietary trans-fats consumed per day was associated with an estimated 0.76 fewer words recalled.

Is this causation or just correlation? The researchers consider that the pro-oxidant (2.) and energetic detriments of dietary trans-fats (3.) are evidence of causation. They used triangulation (4.) with other evidence to ensure that other causal factors were not being mistakenly included. (See charts below if you are interested in the statistical data).

Trans-fats are found in many biscuits, cakes and other processed foods. They are made by pumping hydrogen into liquid vegetable oil so that the oil becomes more solid. Food manufacturers do this in order to increase the shelf life of the products and to improve flavour and texture. You will know that they are present in products if you see the words “partially hydrogenated oils” on the ingredients list.

The leader of this study, Dr Beatrice Golomb, said: “Trans fats were most strongly linked to worse memory, in young and middle-aged men, during their working and career building years…From a health standpoint, trans fat consumption has been linked to higher body weight, more aggression and heart disease…As I tell my patients, while trans fats increase the shelf life of foods, they reduce the shelf life of people.” (5.)

What does this mean for our love affair with biscuits and cakes?

Well, it appears that we love them but they don’t love us. Maybe the best thing to do is to forget about eating them before they make us forget that we have eaten them…


References, Definitions & Data

 1. Beatrice Alexandra Golomb, Alexis K. Bui. June 17, 2015. A Fat to Forget: Trans Fat Consumption and Memory.
 2. Pro-oxidants are substances that accelerate the oxidation of another substance. This process can produce free radicals which are associated with many chronic health problems such as cardiovascular and inflammatory disease, cataract, and cancer. Antioxidants prevent free radical induced tissue damage by preventing the formation of radicals, scavenging them, or by promoting their decomposition. Berries are a great source of antioxidants.
3. Ascherio A, Willett WC. Am J Clin Nutr. 1997 Oct;66(4 Suppl):1006S-1010S. Health effects of trans fatty acids.
4. Triangulation means using more than one method to collect data on the same topic. This is a way of assuring the validity of research through the use of a variety of methods to collect data on the same topic, which involves different types of samples as well as methods of data collection.

Diabetes – The Medical Facts. (WARNING – Disturbing Images)

You hear a lot about diabetes, but you possibly do not get detailed information about the actual processes involved in its development, nor about the specific and, frankly, disturbing consequences of living with this debilitating disease.

This blog goes into some detail and shows some disturbing photos of the results of diabetes. If you do not wish to see these images, you can contact me for a copy of this blog without any images.

I have a very specific reason for covering this issue in such vivid detail: It is no exaggeration to claim that diabetes, particularly but not exclusively type 2 diabetes, is becoming an epidemic in the western world, and not just starting in middle age, but appearing in younger generations. There is solid and reliable evidence that this is due to the western diet – dependent on animal products, low-fibre, high-sugar and fat processed foods, and deficient in whole plant foods.

I will present other articles in defence of this assertion but, for the time being, I want to focus on the disturbing reality of those people who live with diabetes – a largely avoidable chronic disease which has been shown to be both avoidable and reversible by eating a whole food plant-based diet.

Diabetes mellitus (1.)  (DM) is caused by complete absence, relative deficiency of, or resistance to the hormone insulin.

The most common forms of DM are categorised as type 1 diabetes mellitus or type 2 diabetes mellitus.


Type 1 diabetes mellitus

  • previously known as insulin-dependent diabetes mellitus (IDDM)
  • mainly occurring in children and young adults
  • onset is usually sudden and can be life threatening
  • severe deficiency or absence of insulin secretion due to destruction of β-islet cells of the pancreas
  • treatment with injections of insulin is required
  • usually evidence of an autoimmune mechanism that destroys the β-islet cells
  • genetic predisposition and environmental factors, including viral infections. Diet/lifestyle are also implicated

Type 2 diabetes mellitus

  • previously known as non-insulin-dependent diabetes mellitus (NIDDM)
  • most common form of diabetes, accounting for about 90% of cases
  • causes are multifactorial and predisposing factors include:
    • obesity
    • sedentary lifestyle
    • increasing age: predominantly affecting middle-aged and older adults but increasingly affecting younger groups
    • genetic factors
  • onset is gradual, often over many years
  • frequently undetected until signs are found on routine investigation or a complication occurs
  • insulin secretion may be below or above normal
  • deficiency of glucose inside body cells occurs despite hyperglycaemia (high blood sugar) and high insulin level, possibly because of:
    • insulin resistance, i.e. changes in cell membranes that block insulin-assisted movement of glucose into cells.
  • treatment involves diet and/ or drugs, although sometimes insulin injections are required

Pathophysiology (disease processes) (2.) of DM

1. Raised plasma glucose level

After eating a carbohydrate-rich meal the plasma glucose level remains high because:

  • cells are unable to take up and use glucose from the bloodstream, despite high plasma levels
  • conversion of glucose to glycogen in the liver and muscles is diminished
  • gluconeogenesis (non-carbohydrate glucose production) (3.)  from protein, in response to deficiency of intracellular glucose.

2a. Glycosuria (sugar in urine) (4.) and 2b. Polyuria (excessive urination) (5.)

a. Glycosuria results in electrolyte imbalance and excretion of urine with a high specific gravity.

b. Polyuria leads to dehydration, extreme thirst (polydipsia) and increased fluid intake.

3. Weight loss

Cells “starved” of glucose – leading to:

  • gluconeogenesis from amino acids/body protein, causing muscle wasting/tissue breakdown/further increases in blood glucose
  • catabolism of body fat, releasing some of its energy and excess production of ketone bodies (6.)
    • very common in type 1 DM
    • sometimes occurs in type 2 DM

4. Ketosis (7.)and ketoacidosis (8.)

  • generally affects people with type 1 DM –  in absence of insulin to promote normal intracellular glucose metabolism, alternative energy sources must be used instead and increased breakdown of fat occurs. Results in:
    • excessive production of weakly acidic ketone bodies, which can be used for metabolism by the liver
    • ketosis develops as ketone bodies accumulate.
    • excretion of ketones is via the urine (ketonuria) and/ or the lungs giving the breath a characteristic smell of acetone or ‘pear drops’.
    • ketoacidosis develops owing to increased insulin requirement or increased resistance to insulin.
    • if untreated it can lead to:
      • increasing acidosis (↓ blood pH) due to accumulation of ketoacids
      • increasing hyperglycaemia
      • hyperventilation as the lungs excrete excess hydrogen ions as CO2
      • acidification of urine – the result of kidney buffering
      • polyuria as the renal threshold for glucose is exceeded
      • dehydration and hypovolaemia (9.) (↓ BP and ↑ pulse) – caused by polyuria
      • disturbances of electrolyte balance accompanying fluid loss:
        • hyponatraemia (10.) (↓ plasma sodium) and hypokalaemia (11.) (↓ plasma potassium)
        • confusion, coma and death

5, Acute complications of DM

  • Effects and consequences of diabetic ketoacidosis are outlined above
  • Hypoglycaemic coma:
    • occurs when insulin administered is in excess of that needed to balance the food intake and expenditure of energy
    • sudden onset and may be the result of:
      • accidental overdose of insulin
      • delay in eating after insulin administration
      • drinking alcohol on an empty stomach
      • strenuous exercise
      • insulin-secreting tumour
    • Common signs and symptoms of hypoglycaemia include:
      • drowsiness
      • confusion
      • speech difficulty
      • sweating
      • trembling
      • anxiety
      • rapid pulse.
      • May progress rapidly to coma without treatment
      • Rapid recovery with treatment M

6. Long-term complications of DM (Type 1 and type 2)

  • Cardiovascular disturbances
    • DM is a significant risk factor for cardiovascular disorders
    • Blood vessel abnormalities (angiopathies) may still occur even when the disease is well controlled by medication
    • Diabetic macroangiopathy (12.). Most common lesions are:
      • atheroma
      • calcification of the tunica media of the large arteries. Resulting in:
        • Often serious and fatal consequences for Type 1 diabetes at a relatively early age.
        • For both Type 1 and Type 2, the most common consequences are serious and often fatal:
          • ischaemic heart disease (angina and myocardial infarction)
          • stroke
          • peripheral vascular disease.

  • Diabetic microangiopathy (13.). This affects small blood vessels and can result in:
    • thickening of the epithelial basement membrane of arterioles, capillaries and, sometimes, venules. Leading to:
      • Peripheral vascular disease, progressing to gangrene and ‘diabetic foot
      • Diabetic retinopathy (14.)
      • Visual impairment
      • Diabetic nephropathy (15.) and chronic renal failure
      • Peripheral neuropathy (16.) causing sensory deficits and motor weakness
    • Infection
      • DM predisposes to infection, especially by bacteria and fungi, possibly because phagocyte activity is depressed by insufficient intracellular glucose. Infection may cause:
        • boils and carbuncles
        • vaginal candidiasis (17.) 
        • pyelonephritis (18.) 
        • diabetic foot
    • Renal failure
      • This is due to diabetic nephropathy (15.) and is a common cause of death.

  • Visual impairment and blindness
    • Diabetic retinopathy (14.)
      • commonest cause of blindness in adults between 30 and 65 years in developed countries
      • increases the risk of early development of cataracts
      • increase the risk of early development of other visual disorders



  • Diabetic foot
    • Many factors commonly present in DM contribute to the development of this serious situation:
      • disease of large and small blood vessels impairs blood supply to and around the extremities
      • if peripheral neuropathy (16.) is present:
        • sensation is reduced
        • small injury to the foot may go unnoticed, especially when there is visual impairment
        • in DM healing is slower and injuries easily worsen if aggravated, e.g. by chafing shoes
        • often become infected
        • an ulcer may form
        • healing process is lengthy, if at all
        • in severe cases the injured area ulcerates and enlarges
        • may become gangrenous
        • sometimes to the extent that amputation is required.

Why risk or suffer from this truly dreadful disease if the most effective prevention and cure (a WFPB diet) has no side-effects other than improved overall health?

What an unfathomable species we are…




  1. ” Of or pertaining to honey” –
  2. “The physiological processes associated with disease or injury” –
  3. “The metabolic process in which glucose is formed, mostly in the liver, from non-carbohydrate precursors” –
  4. “The presence of sugars (especially glucose) in the urine, often as a result of diabetes mellitus” –
  5.  “The production of an abnormally large amount of urine; one symptom of diabetes” –
  6. “Any of several compounds that are intermediates in the metabolism of fatty acids” –
  7. “A metabolic state in which the body produces ketones to be used as fuel by some organs so that glycogen can be reserved for organs that depend on it. This condition occurs during times of fasting, starvation, or while on a ketogenic weight-loss diet” –
  8. “A severe form of ketosis, most commonly seen in diabetics, in which so much ketone is produced that acidosis occurs” –
  9. “A state of decreased blood volume” –
  10. “An abnormally low concentration of sodium (or salt) in blood plasma” –
  11. “The condition of having an abnormally low concentration of potassium ions in the blood” –
  12. Angiopathy of the larger blood vessels” –
  13. Angiopathy of the small blood vessels” –
  14. “Non-inflammatory disease of the retina” –
  15.  “Damage to, disease of, or abnormality of the kidneys” –
  16. “Any disease of the peripheral nervous system” –
  17. “A fungal infection of any of the Candida (yeast) species” – Also called “thrush”.
  18. “An ascending urinary tract infection that has reached the pelvis of the kidney” –

Main source of material: Waugh, Anne; Grant, Allison. Ross & Wilson Anatomy and Physiology in Health and Illness E-Book (p. 236-8). Elsevier Health Sciences. Kindle Edition.

Weight Loss – Down to Exercise or Diet?

You have probably heard Michelle Obama and many others telling overweight people that they can drop their extra pounds by picking up their running shoes. But is this really the answer to the increasing epidemic of obesity spreading around the world?

An Instructor from T Colin Campbell’s Centre for Nutrition Studies considers that her personal experience suggests that this is simply NOT the answer…

Healthy Weight Loss = 80% Nutrition + 20% Exercise


 appeared in the 1998 edition of Shape magazine as one of their “Success Stories” for weight loss.

She was engaged in “an excruciating exercise program of power walking/jogging 35-40 miles per week, plus an additional 20 miles on the bike.” Of course she lost weight, but as the years passed she found that the unwelcome pounds came creeping back.

She read an article that, at the time, seemed to explain why this might be happening: “…as we age, our metabolism slows down due to natural muscle mass decreases, so we need to increase our calorie burning exercise. If we don’t, we gain 10 lbs every few years, even though we are still exercising.”

Discouraged by the thought of having to continually ramp up the extreme exercise as each year passed, she found that her health started to decline – “…high cholesterol, high blood pressure, swollen and painful joints, and hormonal issues. I was only in my forties, and my lack of health had become a source of great stress. I couldn’t imagine what I would be like in my 60’s. My joints already hurt so much!”

Eventually, she came across the landmark documentary film Forks Over Knives. Things changed from then on. And she was not alone. This very film revolutionised my life and the lives of many people I come across daily.

Terri, like many, many others, learned that optimal health was not about exercising more. Rather, it was about eating the right foods. “Not chicken and fish like I had thought, but whole grains, legumes, vegetables, and fruits!”

  • Leanest cut of beef ~28% calories from fat
  • Skinless chicken breast ~ 24% from fat
  • Tuna ~21% from fat
  • Salmon ~ 40% from fat
  • Eggs ~70% from fat!

Nutrition is Key

Even though she continued to consider that exercise and stress management are important “…the real key—80% of the equation—is nutrition – in particular, eating plants.

Now, her main exercise is walking the dog daily for around 30-45 minutes with some gentle yoga four days a week – without the dog, I guess!

She says that her cholesterol levels have dropped and she no longer suffers from inflammation or pain.

While exercise and stress management are “…very important pieces to the health puzzle; it’s not whole without them. But, nutrition is the biggest piece of the picture. “You can’t outrun your fork.” “

Some edited thoughts (1.) from Dr. Greger

The food industries like to blame inactivity as the prime cause of obesity, not the promotion and consumption of their calorie-rich products. (2.) On the contrary, however, research suggests that the level of physical activity may have actually increased in the United States over the past few decades. (3.) We know that obesity is rising even in areas where people are exercising more. (4.) This is likely explained by the fact that eating activity levels are outstripping physical activity levels. (5.)…Researchers who accept grants from the Coca-Cola Company (6.) call physical inactivity “the biggest public health problem of the 21st century.” (7.) Actually, physical inactivity ranks down at number five in terms of risk factors for death in the United States and number six in terms of risk factors for disability. (8.) And inactivity barely makes the top ten globally. (9.)

diet is by far our greatest killer, followed by smoking. (10.)

Of course, that doesn’t mean you should sit on the couch all day…. in addition to helping you enjoy a healthy body weight, exercise can also ward off and possibly reverse mild cognitive decline, boost your immune system, prevent and treat high blood pressure, and improve your mood and quality of sleep, among many other benefits.


  1. Greger, Michael; Stone, Gene. How Not To Die: Discover the foods scientifically proven to prevent and reverse disease (Air Side Edt) (p. 393). Pan Macmillan. Kindle Edition
  2. Freedhoff Y, Hébert PC. Partnerships between health organizations and the food industry risk derailing public health nutrition. CMAJ. 2011;183( 3): 291– 2.
  3. Westerterp KR, Speakman JR. Physical activity energy expenditure has not declined since the 1980s and matches energy expenditures of wild mammals. Int J Obes (Lond). 2008;32( 8): 1256– 63.
  4. Dwyer-Lindgren L, Freedman G, Engell RE, et al. Prevalence of physical activity and obesity in US counties, 2001– 2011: a road map for action. Popul Health Metr. 2013;11: 7.
  5. Laskowski ER. The role of exercise in the treatment of obesity. PMR. 2012;4( 11): 840– 4.
  6. Archer E, Hand GA, Blair SN. Correction: Validity of U.S. Nutritional Surveillance: National Health and Nutrition Examination Survey Caloric Energy Intake Data, 1971– 2010. http:// plosone/ article? id = 10.1371/ annotation/ c313df3a-52bd-4cbe-af14-6676480d1a43. October 11, 2013. Accessed April 23, 2015.
  7. Blair SN. Physical inactivity: the biggest public health problem of the 21st century. Br J Sports Med. 2009;43( 1): 1– 2.
  8. Murray CJ, Atkinson C, Bhalla K, et al. The state of US health, 1990– 2010: burden of diseases, injuries, and risk factors. JAMA. 2013;310( 6): 591– 608.
  9. Lim SS, Vos T, Flaxman AD, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990– 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012;380( 9859): 2224– 60.
  10. Murray CJ, Atkinson C, Bhalla K, et al. The state of US health, 1990– 2010: burden of diseases, injuries, and risk factors. JAMA. 2013;310( 6): 591– 608.


Joe’s Final Comment

For many years I also considered that exercise was the main answer. I would train for marathons, work myself into the ground – pushing my body so hard that I repeatedly wrecked my muscles and joints; but still I would find that my unwanted weight crept back, and those damned “love handles”  would never disappear.

Now, at the age of 56, my body feels like it is at its optimal weight – the lowest level since I was in my teens. I never go hungry or actively control the quantity of food I eat – and I eat A LOT!

Before “going cold turkey” into a WFPB diet, I was starting to feel old and pretty pessimistic about my future, even though I was very conscious of my dietary intake and had been a vegetarian on and off for most of my life.

Now, my arthritis has all but disappeared. My joints no longer ache. I no longer get constipated or have the recurrent mouth ulcers and nose bleeds that I had for years. Getting in and out of the car, or up from sofas, no longer causes exclamations of pain. I feel like I have more energy now than I had years ago. My mental attitude is consistently positive and…I am really looking forward to the future.

Of course my and Terri’s claims about the health benefits of a WFPB diet are merely anecdotal; but without a personal experience of the power of plant-eating I would not be able to recommend it to other people. I just wish my parents had been able to enjoy its health benefits instead of the lingering and painful diet-related diseases that they endured.

If you have a personal story that you think would inspire others, let me know.