What Happens When You Eat a Bowl of Kellogg’s Frosties?

Further to recent blogs on breakfasts 1 and the ‘bliss point’ in processed foods 2 , I thought it would be interesting to take a more detailed look inside the body, just to see what actually happens when a highly processed sugary product, specifically Kellogg’s Frosties, meets the inside of a human body – touching on associated issues, ranging from insulin resistance and cellular respiration to diabesity and non-alcoholic fatty liver disease.

Grrreat for whom?

It’s quite true that such breakfast cereals are great for the manufacturer’s profit and loss account, but what’s their true cost in terms of human health?

In order to understand what happens to those sweet, crunchy morsels once they get into our bodies, we’ll need to delve into a bit of nutritional science. So here goes…

Frosties – ingredients & nutritional information

As you will see from the footnote below 3 , a 100 g of Frosties contains 87 g processed carbohydrates, 37 g of which is pure sugar (specifically, sucrose – a disaccharide consisting of one glucose and one fructose molecule). The carbohydrates are processed to remove nearly three quarters of the fibre contained in the original whole corn (also called maize) – 2 g/100 from 7-8 g/100 g in whole corn. This gives Frosties a glycaemic index (GI) of 51 compared to 100 for pure glucose 4 . To its credit, Frosties is at least fortified with several vitamins and doesn’t contain any palm oil.

From mouth to bloodstream

As soon as Frosties enter the mouth, the carbohydrate-digesting enzyme amylase produced in saliva starts to break down the sucrose into its two monosaccharides, glucose and fructose, and the lump of food in the mouth is then referred to as a ‘bolus’.

From the mouth, the bolus passes to the stomach, during which time it magically changes its name to ‘chyme’ – a pulpy acidic fluid consisting of gastric juices and partly-digested food.

From the stomach, the chyme passes into the first part of the small intestine, the duodenum.

A signal then passes to the pancreas for it to release pancreatic amylase along a duct and into the duodenum.

At this point, a number of enzymes have pretty much completed the digestion of the sugars and any starches, producing the end product of the monosaccharide, glucose.

The resulting glucose within the mixed contents of the intestine (the ‘lumen’) then passes through the wonderfully complex epithelial membrane and into the bloodstream through an absorption process called ‘active transport’.

Here comes the insulin – hopefully…

Once the glucose levels rise in the bloodstream, the beta cells of the islets of Langerhans within the pancreas detect this increase and release the hormone, insulin – in healthy individuals, that is.

The situation is different for those with type 1 diabetes (T1D), where the pancreas does not produce insulin (or only very small quantities).

For those with type 2 diabetes (T2D), the situation is not the same, since plenty of insulin may be released from the pancreas but, for reasons covered below, fails to do its job properly.

If blood glucose levels are too low, another hormone called glucagon is released into the bloodstream, this time from the alpha cells in the islets of Langerhans within the pancreas.

Glucagon’s function is to instruct the release of some glucose which has been stored as glycogen in the liver and muscle cells (a process called glycogenolysis).

This is just one of the wonderful examples of homeostasis – a continual balancing act occurring within our bodies every second of every day. Put simply:

  • when blood glucose levels rise above a certain level, the pancreas produces more insulin
  • when blood glucose levels fall below a certain level, insulin production stops and glucagon production starts

From blood to cell

In our scenario, the sugar in the Frosties has been converted into glucose and has ended up in the bloodstream. Insulin’s main job now is to get that glucose into the body’s cells. If it does so successfully – and this is the big IF when it comes to those with T2D – the glucose is oxidised in the cells (that is, the glucose combines chemically with oxygen) and becomes a source of energy. This intracellular energy-production process is known as ‘cellular respiration’.

Cellular respiration (also known as internal respiration) is a complex process, involving three metabolic pathways: glycolysis, the citric acid (Krebs) cycle, and oxidative phosphorylation; but the important result is that the glucose from our Frosties is converted into energy. This energy is in the form of ATP (adenosine triphosphate), known as the “molecular (or energy) currency” of intracellular energy transfer. This only takes place within cells,  mostly within the mitochondria (the ‘energy factories’) but also, to a lesser degree, within the cytoplasm of the cell. The product is the energy our bodies require for every function.

If there’s any excess glucose which is not required immediately, it will get stored as glycogen in the liver or skeletal muscles for future use (a process rather confusingly called glycogenesis – the reverse process to glycogenolysis).

If you’re interested in a little more detail on the process of carbohydrate metabolism not covered above, see the note 5 below.

Now comes the spike

If glycogen reserves in the liver are saturated, the excess glucose gets converted into fat for long-term storage in the adipose (fat) tissues – beneath the skin (subcutaneous fat), around internal organs (visceral fat) and in bone marrow (yellow bone marrow).

Because Frosties contain highly refined carbs, rather than the complex starchy carbs found in whole plants, the glucose is released very rapidly. Basically, the more processed the carbs, the quicker they end up as glucose in the bloodstream. Thus, the Frosties are likely to cause what is called an initial ‘insulin spike‘.

In the long term:

  • insulin spikes can cause serious and irreversible damage to organs, nerves, and blood vessels
  • there’s likely to be an excess of glucose produced as a result of eating such foods as Frosties – unless you’re running fast on a treadmill when you’re eating! This means that regular consumption may lead to increased body fat and all the health problems associated with that

In the short term:

  • the sudden hit of these simple carbs (the ‘sugar rush‘) is likely to upset the delicate balance in the blood sugar level and is known to cause some fluctuations in energy levels and mood over the following hours – which could leave the person irritable and tired as the ‘sugar crash‘ arrives and glucose levels settle back to normal
  • it’s also likely that the person will feel hungry again very soon, since they didn’t get enough of the other nutrients to sustain energy, like protein and fibre
  • while eating the Frosties, the person’s brain would have responded to the sugar by creating a surge of the “feel-good” brain chemicals dopamine and serotonin. This also happens with certain drugs, such as cocaine. In a similar way to a drug, the body craves more after the initial high. This is one of the reasons that it is very much easier to overeat simple carbs, while complex starchy carbs don’t have the same effect

When the spikes have burst the insulin bubble

Prediabetes 6 – arguably a disease in itself – usually takes a number of years to develop into full-blown T2D, where muscle and other cells stop responding to insulin. Known as insulin resistance, this condition causes blood sugar and insulin levels to stay high long after eating. The excessive demands made on the insulin-making cells can eventually wear them out so much that insulin production can eventually cease. 7

Insulin resistance & diabetes

Before pinning down what insulin resistance is, we probably need to be clear on just what diabetes is.

As far back as a 1927 study 8 , a clear link between diabetes and fat consumption was demonstrated. In this study, young, healthy people were split into two groups: half were put on a fat-rich diet, and the other half were put on a carb-rich diet. Within just two days, glucose intolerance rose alarmingly in the fat-rich group, with twice as much blood sugar as the carb-rich group. The same principle revealed in this study has been duplicated and confirmed ever since, namely:

  • as fat in the diet rises, blood sugar spikes rise

Why is this? As it happens, it took around seven decades before the answer could be provided and, thus, form the basis of the current understanding of the cause of T2D. In basic terms, fat in the cells blocks insulin from being able to usher glucose into the cells to be used as energy. As a result of this, the sugar stays in the bloodstream, eventually filling available organs and muscle cells with fat, and reaping havoc on the body as a whole.

Every vampire needs an invitation

“Prepare ye the way for the Lord”!

I think it was Dr Greger who drew the comparison between blood sugar (glucose) and vampires. Just as a vampire requires an invitation before entering private homes, glucose needs an invitation before it can enter our cells. Within our bodies, that invitation comes in the form of insulin.

When a cell requires additional energy, it binds to one of the insulin molecules passing by in the bloodstream and that molecule binds to a specific insulin receptor on the surface of the cell membrane. Once there, the insulin acts like a key, opening up a ‘gap’ in the cell membrane – through the release of a number of enzymes – so that glucose, also circulating in the bloodstream, can enter the cell. It’s important to understand that there’s no other way that glucose can enter the cell than through this insulin receptor.

Glucose (C6H12O6) is a large molecule with 6 carbon atoms. As such. it’s too big to get into the cell through simple diffusion. This is why it needs its own John the Baptist (insulin) to ‘prepare the way for the load‘. The term used for this is ‘facilitated diffusion‘ (also known as ‘facilitated transport’) and it happens down a concentration gradient – that is, it will only happen when there’s more glucose outside the particular cell than there is inside it. If the cell has sufficient glucose inside already, it will close up the insulin receptor and no more glucose will get inside, until more is required.

This form of glucose transport within our muscles is responsible for clearing around 85% of the glucose from our blood.

By the way, all of this is something a simplification of the whole process, of course. In actual fact, even the insulin receptor (one of many different types of cell receptors) has multiple additional roles in physiological processes within us.

The diagram below 9  gives a brief overview of this complexity (sometimes referred to as pleiotropy – where one gene affects other seemingly unrelated traits).

Insulin through its receptor affects multiple physiological processes in the organism (left) by increasing (green arrows) or decreasing (red arrows) various intracellular metabolic pathways (right).

Time to call the locksmith

All well and good, but if the pancreas doesn’t produce insulin (as in T1D) then our muscle cells don’t get any energy, no matter how much glucose is floating around in the bloodstream, because there’s no key (insulin) to open the lock (insulin receptor in the cell membrane). This is why sufferers of T1D have to have insulin injections (the locksmith), otherwise blood sugar levels would simply rise and rise and eventually result in death. A person with T1D will have to monitor their blood sugar levels very carefully if they’re in the habit of eating bowls of Frosties – a habit which would not be recommended by any medical expert.

When the fat hits the fan

But what about T2D, where there’s still plenty of insulin being released into the bloodstream from the pancreas – at least, until later stages of untreated/unreversed 10 diabetes? If our muscle cells are so full of intramyocellular lipids (fat stored as a result of less-than-ideal dietary habits, where sugary foods like Frosties and high-saturated fat products have been eaten over extended periods of time), the key won’t be able to open the lock – again, no matter how much insulin and glucose might be available. The result is similar to T1D: blood sugar levels can rise and rise11

Dr Greger explains this process in more detail in his video, “What Causes Insulin Resistance?” 12 .

Diabesity

The link between obesity and diabetes (so strong now that the term ‘diabesity’ 13 has been coined) can be explained by realising that the fat spilling into the bloodstream from fat cells in obese individuals can get lodged in the very muscle cells we’ve been talking about. This then leads to insulin resistance and the onset of T2D.

So, although Frosties contain very little fat (only 0.6%), if the person eating them is already obese, the blood glucose quickly resulting from their consumption will end up in the bloodstream and find that the muscle cells are already fully or partially blocked by the intracellular fat 14 . Some of the glucose will be stored as further fat deposits, while some will continue to circulate in the bloodstream.

Non-alcoholic fatty liver disease

In T2D, the pancreas has been pumping out more and more insulin in an effort to overcome the fat induced insulin resistance in muscle cells. Over time, these high blood insulin levels can lead to accumulation of fat in the liver – non-alcoholic fatty liver disease (NAPFD).

Before the final diagnosis of T2D, the liver will certainly be protesting, without its owner ever hearing its silent screams. But eventually, this fat build up in the liver will make it, too, resistant to insulin in the same way as it does with the muscles.

Breakfast & the liver

Between meals, a normal liver will constantly be turning its stores of glycogen into glucose, which it then pumps into the blood to keep the brain alive; and when we do eat breakfast, after a night without dietary intake, the insulin released from the meal should turn off liver glucose production. However, if there’s too much fat in the liver, it fails to respond to that breakfast signal.

The twin vicious cycles of diabetes 15

Cycle #1

The fatty liver continues pumping out glucose all day long, on top of whatever we’re eating. The pancreas responds to the high level of blood sugar by releasing more insulin, causing the liver to get fatter and fatter. Meanwhile, fatty muscles (i.e. muscle cells that have been stuffed with surplus fat), within the context of eating too many calories, leads to the fatty liver getting even fattier.

And this all starts before diabetes is even diagnosed. This is why it’s a mistake to under-estimate the danger of being prediabetic.

Cycle #2

Fatty liver can be fatal and, because our bodies do all they possibly can to keep us alive (in spite of the relentless pressure we may impose on them), the liver tries to offload the fat by dumping it back into the bloodstream in the form of VLDL (very low density lipoprotein). This then finds its way into the beta (or so-called eyelet) cells of the pancreas, making it into a fatty pancreas – thereby destroying the ability of the pancreas to produce insulin. Blood sugar levels go up and up, leading to hyperglycemia – damaging the vessels supplying blood to vital organs, increasing the risk of heart disease, stroke, kidney disease, vision loss and irreversible nerve damage, gangrene, amputations and, of course, death.

Thus, by looking at these two cycles, it’s possible to see how T2D diabetes develops and to understand how it is a condition of excess fat inside our organs.

Final thoughts

Just eating the odd bowl of Frosties isn’t, of course, going to lead to diabesity; but if we tell ourselves that eating such foods “isn’t really all that bad” (they are, after all, fortified with added vitamins and minerals!), then we’re also likely to justify eating a whole load of other processed foods. And it’s the combination of these fatty, sugary, salty, processed foods being eaten over extended periods of time that ends up causing serious diet-related diseases.

Another important aspect is that every time we choose such unhealthy foods, we establish habits and addictions that can keep us locked in to vicious cycles – starting with those silent screams within, but ending up with very apparent indications of harm that’s already been done.

I think I’ll give Mr Kellogg’s offerings a miss.

You may want to have a go at the brief quiz below…


Quick Quiz - Diabetes

(All answers are contained in the article.)

1.

Where is leptin produced in the body? 

2.

Ghrelin ........... appetite.

3.

Leptin resistance cannot happen if there is plenty of leptin in the bloodstream. True/False?

4. What's perhaps the best way of increasing the effectiveness of leptin?

References

  1. Breakfast Confusion []
  2. Bliss Points, Pleasure Traps & Wholefood Plant-Based Diets []
  3.  Source: Waitrose. []
  4. GI of Frosties. []
  5. A little more information on carbohydrate metabolism: Not all cells in the body are the same in relation to their requirements for glucose and only glucose. Erythrocytes (red blood cells) and neurones (brain cells) can use only glucose for fuel. This means that the maintenance of blood glucose levels is vital to ensure the provision of a constant energy source to these cells.

    Most other cells can also use other sources of fuel (amino acids, fatty acids, glycerol and occasionally nucleic acid) in a process called gluconeogenesis.

    So, while some glucose is transported to the liver (to satisfy its own significant energy requirements), and some will be oxidised in other cells around the body, a certain level of glucose has to remain in the circulating blood to maintain the normal blood glucose of about 3.5– 8 mmol/ L (63– 144 mg/ 100 ml). If there is excess glucose above blood level requirements, insulin will convert it to the insoluble polysaccharide, glycogen, in the liver and in skeletal muscles.

    Glycogen is the main storage form of glucose in animal cells. In humans, most glycogen is found in the liver (10% of the liver mass), with muscles only containing a relatively low amount (1% of the muscle mass), and small amounts of glycogen also being stored in some glial cells in the brain.

    Inside cells, glycogen-formation is a means of storing carbohydrate without upsetting osmotic equilibrium. However, before it can be used to maintain blood levels or provide ATP, it has to be broken down again into its constituent glucose units.

    Liver glycogen stores constitute a store of glucose used for liver activity and to maintain the blood glucose level.

    Muscle glycogen stores provide glucose requirements of muscle activity.

    Glucagon isn’t the only hormone associated with the breakdown of glycogen to glucose, adrenaline (epinephrine) and thyroxine are are also involved. Naturally, if there is an excess of carbohydrate, above that required to maintain blood glucose level and glycogen stores in the tissues, it will be converted to fat and stored in the fat depots around the body.

    This is just a glimpse at the complex world of carb metabolism, and doesn’t even touch on the metabolism of the other two macronutrients, protein and fat. If you want to delve deeper into this subject, I can recommend the following introductory book: Ross & Wilson Anatomy and Physiology in Health and Illness. 2018 edn. Anne Waugh BSc(Hons) MSc CertEd SRN RNT PFHEA (Author), Allison Grant BSc PhD FHEA. []

  6. Dr Michael Greger Podcast – start at 6:30 mins – The Latest on Children’s Health. []
  7. Hocking S, Samocha-Bonet D, Milner K-L, Greenfield JR, Chisholm DJ. Adiposity and insulin resistance in humans: the role of the different tissue and cellular lipid depots. Endocr Rev. 2013 August; 34(4): 463-500. []
  8. J Shirley Sweeney. DIETARY FACTORS THAT INFLUENCE THE DEXTROSE TOLERANCE TEST A PRELIMINARY STUDY. JAMA Int Med, Dec, 1927, Vol 40, No. 6. []
  9. Endotext: The Insulin Receptor and Its Signal Transduction Network
    Pierre De Meyts, MD, PhD, F.A.C.E. []
  10. Diet Reverses Type 2 Diabetes – How Long Have We Known This? []
  11. Roden M. How free fatty acids inhibit glucose utilization in human skeletal muscle. News Physiol Sci. 2004; 19: 92-96. []
  12. What Causes Insulin Resistance by Michael Greger M.D. FACLM January 6th, 2017 Volume 33. []
  13. Diabesity Hardcover – 1 Oct 2004 by Francine R., MD Kaufman []
  14. Estadella D, da Penha Oller do Nasciment CM, Oyama LM, Ribeiro EB, et al. Lipotoxicity: effects of dietary saturated and transfatty acids. Mediators Inflamm. 2013: 137579. doi: 10.1155/2013/137579. Epub 2013 Jan 31. []
  15. Diabetes as a Disease of Fat Toxicity. Michael Greger M.D. FACLM April 8th, 2015 Volume 24 []

Diabetes – Wheat VS Chickpea & Lentil Pasta

You’ve probably seen these relatively new additions to the dried pasta ranges – lentil fusilli, chickpea penne, etc. Are they just another marketing fad with no health benefits over the usual wheat pasta, or do they provide some of the same health benefits for which lentils and chickpeas are well known? Let’s see…

What’s the problem anyway?

Well, it’s no secret that eating traditional wheat pasta, especially non-wholemeal, isn’t the best option if you want to maintain low postprandial blood glucose (BG) responses – important since repeated postprandial hyperglycaemia 1 is an early abnormality of glycaemic control  2 associated with type 2 diabetes 3 . Basically, if you don’t want to help yourself to diabetes, then avoid helping yourself to too much white flour in bread or in pasta.

Benefits of lentils and chickpeas

Frequent consumption of whole pulses, the edible seeds of legumes or pod-bearing plants, including beans, chickpeas, yellow peas and lentils 4 , is associated with a higher-quality diet 5 6  lower body weight 7  and improved markers of long-term glycaemic control 8 . Important for our current investigation, whole pulses lower postprandial glycaemic response 9 10 11 12 13 14reduce hunger 13 15 16 17 18 and suppress food intake 13 14  up to 2-6 hours following their intake. Of these benefits, reduced blood glucose (BG) oscillations are of particular importance 19 .

Whole VS Powdered

The chickpeas and lentils are dried and powdered into a flour before being made into the various pasta shapes you buy in the shops. But surely this processing affects the fibre structure and hence the ability that the whole beans/pulses had for keeping blood glucose levels relatively stable after meals? apparently not so.

Study results

A 2014 study 20 took healthy males and tested whether consumption of these powdered chickpeas and lentils would produce the same blood glucose response as whole chickpeas and lentils. They also compared results with a control group consuming wheat-based pasta.

They concluded that: “commercial processing of pulses to a powder form does not alter their low glycaemic characteristics. Pulse powders can therefore be used as value-added ingredients in home cooking and functional foods to improve postprandial glycaemic control. It is expected that the development of such foods will help promote consumption of pulses in convenience foods among individuals who normally avoid them due to taste or perceived inconvenience.

Final thoughts

There are some pretend healthier products out there, such as the “spinach trottole” which only has 1% spinach and 99% wheat! Okay, wheat pasta won’t kill you, and there are much worse foods for the maintenance of blood glucose levels – such as white bread. But it’s good to know that you can get some of the well-known health benefits of beans & pulses such as chickpeas and lentils in pasta form – especially when they are so easy and quick to cook and serve.

Naturally, the best way to get all the antioxidant power from beans and pulses is to eat them as whole foods. There’s no better way to maintain your health than including whole beans and pulses in your meals every day. This is why they form part an integral part of Dr Greger’s Daily Dozen 21 . I prefer to soak them overnight then stick them in the pressure cooker for 15-20 mins, depending on the bean/pulse. Then they’re ready to add to any meal or simply act as a snack you can grab from the fridge whenever you’re peckish.


References

  1. Definition of postprandial hyperglycaemia – Diabetes Self-Management. []
  2. Glycaemic control: Glycaemic control in diabetes BMJ 1999. []
  3. Association AD (2001) Postprandial blood glucose. American Diabetes Association. Diabetes Care 24, 775–778. []
  4. Pulse Canada (2012) Canada’s pulse industry in the global market. []
  5. Mitchell DC, Lawrence FR, Hartman TJ, et al. (2009) Consumption of dry beans, peas, and lentils could improve diet quality in the US population. J Am Diet Assoc 109, 909–913. []
  6. Mudryj AN, Yu N, Hartman TJ, et al. (2012) Pulse consumption in Canadian adults influences nutrient intakes. Br J  Nutr 108, Suppl. 1, S27–S36. []
  7. Papanikolaou Y & Fulgoni VL 3rd (2008) Bean consumption is associated with greater nutrient intake, reduced systolic blood pressure, lower body weight, and a smaller waist circumference in adults: results from the National Health and Nutrition Examination Survey 1999–2002. J Am Coll Nutr 27, 569–576. []
  8. Sievenpiper JL, Kendall CW, Esfahani A, et al. (2009) Effect of non-oil-seed pulses on glycaemic control: a systematic review and meta-analysis of randomised controlled experimental trials in people with and without diabetes. Diabetologia 52, 1479–1495. []
  9. Jenkins DJ, Wolever TM, Taylor RH, et al. (1980) Exceptionally low blood glucose response to dried beans: comparison with other carbohydrate foods. Br Med J 281, 578–580. []
  10. Jenkins DJ, Wolever TM, Taylor RH, et al. (1981) Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 34, 362–366. []
  11. Foster-Powell K, Holt SH & Brand-Miller JC (2002) International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr 76, 5–56. []
  12. Wong CL, Mollard RC, Zafar TA, et al. (2009) Food intake and satiety following a serving of pulses in young men: effect of processing, recipe, and pulse variety. J Am Coll Nutr 28, 543–552. []
  13. Mollard RC, Wong CL, Luhovyy BL, et al. (2011) First and second meal effects of pulses on blood glucose, appetite, and food intake at a later meal. Appl Physiol Nutr Metab 36, 634–642. [] [] []
  14. Mollard RC, Zykus A, Luhovyy BL, et al. (2011) The acute effects of a pulse-containing meal on glycaemic responses and measures of satiety and satiation within and at a later meal. Br J Nutr 108, 508–517. [] []
  15. Pai S, Ghugre PS & Udipi SA (2005) Satiety from rice-based, wheat-based and rice-pulse combination preparations. Appetite 44, 263–271. []
  16. Sparti A, Milon H, Di Vetta V, et al. (2000) Effect of diets high or low in unavailable and slowly digestible carbohydrates on the pattern of 24-h substrate oxidation and feelings of hunger in humans. Am J Clin Nutr 72, 1461–1468. []
  17. Leathwood P & Pollet P (1988) Effects of slow release carbohydrates in the form of bean flakes on the evolution of hunger and satiety in man. Appetite 10, 1–11. []
  18. Holt SHA (1995) A satiety index of common foods. Eur J Clin Nutr 49, 675. []
  19. Ceriello A, Colagiuri S, Gerich J, et al. (2008) Guideline for management of postmeal glucose. Nutr Metab Cardiovasc Dis 18, S17–S33. []
  20. Anderson GH, Liu Y, Smith CE, et al. The acute effect of commercially available pulse powders on postprandial glycaemic response in healthy young men. Br J Nutr. 2014;112(12):1966-1973. []
  21. Dr Greger’s Daily Dozen. []

Vegetarian Diets and the Risk of Diabetes

A September 2018 review 1 looked at whether the dramatic worldwide increase in cases of type 2 diabetes (T2DM – type 2 diabetes mellitus) could be slowed down if individuals made simple dietary changes rather than seeking solutions through medication.

Summary

The reviewers note that vegetarian diets are inversely associated with risk of developing diabetes, and this is independent of the positive association of meat consumption with diabetes development.

Range of diets

Vegetarian diets range* from:

  • vegan (no animal products)
  • lacto-ovo-vegetarian (no animal meat, but consumes milk and eggs)
  • pesco-vegetarian (consumes fish)
  • semi-vegetarian/flexitarian (occasional meat consumption)

*N.B. This review does not look at WFPB or non-SOS WFPB diets.

The most important aspects of any of these types of diets is the emphasis on:

  • whole grains
  • fruits and vegetables
  • legumes
  • nuts
  • reduction of saturated and trans fats

Problem – what problem?

Oh there’s a big problem, alright. Diabetes has now reached epidemic levels, with an estimated 451 million cases worldwide in 2017 – a number that is predicted 2  to increase to 693 million by 2045.

Where’s the evidence?

About 90% of diabetes diagnoses are type 2 (T2DM) – all of these appear to be lifestyle-related 3 . Additionally, the lifestyle factor most linked to improvements in protection against, treatment of and cure for is diet – with the take-home facts being that animal foods encourage whist plant foods discourage T2DM 4 .

As countries develop a more Westernised diet (also known as the SAD or Standard American Diet), the rates of diabetes within those countries increases 3 .

Omnivores vs Vegetarians

A diet differing from the typical Westernised diet is a vegetarian one.  The results of changing to a vegetarian diet is clear. For instance, research 3 shows that vegetarians in the US have a lower prevalence of diabetes than omnivores (that is, those who consume both plant and animal foods, although much more of the latter than the former foods in the case of modern Westernised diets). Other research 5 6 7 8 9  backs up the proposition that a vegetarian diet is significantly better for the prevention and treatment of diabetes than an omnivore diet.

To the heart of the matter

People with diabetes have a 2–4 times greater risk of suffering from CVD (cardio-vascular disease) 10  . Even those who just adhered to a lacto-ovo-vegetarian diet have been shown 11  to have significantly decreased CVD risk factors, specifically blood pressure, serum cholesterol, and blood glucose levels than those adhering to an omnivorous diet.

Another 2013 study 12  examined ischaemic heart disease risk of vegetarians versus non-vegetarians in a large British sample of 44,561 individuals. They found that vegetarians had a lower BMInon-HDL cholesterol, and systolic blood pressure than the non-vegetarians.

Other risks with diabetes

When looking at other diabetes risk factors and comorbidities, a 2015 study 13 found that those adhering to a vegan diet supplemented with vitamin B12 had a significantly larger decrease in neuropathic pain 14 than the control group receiving just B12 supplementation.

A 1988 study 15 examined patients who had diabetic neuropathy 16  and renal failure who followed a vegan diet for 12 months found significant improvements in the following:

  • creatinine clearance 17
  • urine protein levels
  • cholesterol levels
  • blood glucose levels

Is it too late for me?

Okay, if you’ve eaten a vegetarian diet from childhood, you are less likely to have developed diabetes; but what if you’ve been stuffing in the eggs and bacon, doughnuts and cream cakes for most of your life – is it too late? Another 2018 study 18 found that adopting a vegetarian diet later on in life can greatly reduce diabetes risk, showing the benefits of using a vegetarian diet in an intervention. Other research studies 19 20 21    show the same positive results of dietary changes later in life.

Medication vs diet

There’s also evidence 22 23 24 25 supporting the suggestion that adopting a vegetarian diet is more effective than at improving diabetes symptoms than traditional medication. Of course, packing in smoking and getting lots of exercise are also significantly important lifestyle factors that can prevent and treat diabetes.

Physical and mental benefits

A 2013 study 26 looked at the psychological effects of adopting a vegetarian diet. The investigators assessed the following:

  • quality of life
  • eating behaviour
  • depressive symptoms

They divided diabetic subjects into vegetarian and non-vegetarian groups and found an increase in quality of life and decrease in depressive symptoms in the vegetarian group. Regarding dietary restraint, the vegetarian group was was able to show an increased ability to resist the ‘temptation’ to eat more food and more unhealthy food than the non-vegetarian group.  This study showed that adopting a vegetarian diet has both physical and psychological benefits for T2DM patients.

Not all vegetarian diets are equal

Some vegetarians live on processed foods, crisps, chips and sweets. Some hate all vegetables (except fried white potatoes!) while others eat largely whole plant foods.

To examine the differences in type 2 diabetes risk of vegetarians who consume an unhealthy diet (characterised by refined grains, starchy foods, added sugars, low fruits and vegetables) or healthy diet (characterised by whole grains, fruits, vegetable, legumes), a 2016 review 27 categorised the latter as hPDI (a Healthful Plant-Based Diet) and uPDI (an Unhealthy Plant-Based Diet Index) in order to distinguish between healthy and unhealthy plant foods being eaten.

Thus, hPDI assigned positive scores to:

  • whole grains
  • fruits
  • vegetables
  • nuts
  • vegetable oils
  • tea and coffee

and reverse scores to:

  • fruit juices
  • sweetened beverages
  • refined grains
  • potatoes (white)
  • sweets
  • desserts
  • animal foods

The uPDI used the opposite approach.

The results were pretty clear: PDI and hPDI were inversely associated with T2DM, and the uPDI was positively associated with T2DM. This shows the benefit of following a vegetarian diet that is high in whole grains, vegetables, fruits, nuts, and legumes in preventing T2DM.

Study conclusions

The researchers in this September 2018 review 1 drew the following conclusions:

  • the role of all types of vegetarian diets in the prevention and treatment of diabetes is well established
  • clinicians and healthcare providers should feel confident in recommending a vegetarian diet to their patients who have pre-diabetes or T2DM
  • the type of foods that should be consumed while following this diet is critical to achieve the therapeutic effects
  • a vegetarian diet that is high in unhealthy foods such as refined grains, saturated fats, and added sugars is positively associated with T2DM
  • a vegetarian diet that is high in healthy foods such as whole grains, fruits, vegetables, nuts, legumes, and unsaturated fats is negatively associated with T2DM

Final thoughts

It’s pretty obvious to all reasonable people who’ve done even a bit of research that a significant solution to diabetes (prevention, management and cure) lies in simple dietary changes (as well as dropping the tobacco and picking up the weights instead).

However, while this review does look at different manifestations of vegetarian diets, it does not cover in detail how much more effective a completely WFPB (ideally a non-SOS WFPB) diet is when compared with the rest of the vegetarian offerings. Naturally, it hints at this through its mention of the above-mentioned 2016 review 27

If you look online or go to a vegetarian/vegan restaurant and look at what often goes into their recipes you will soon understand what I’m getting at. A quick glance at the menus of one vegan restaurant 28 local to me reveals the potentially unhealthy ingredients and cooking methods that can be both plant-based and unhealthy at the same time –  ‘double fried chips and a pot of garlic mayo‘  and ‘Sticky Toffee Pudding served with a caramel glaze‘ will only offer limited assistance, if any, to diabetic customers looking for the healthy alternative to bangers and mash!

Of course, as evidenced in this review, going plant-based rather than relying on pharmaceuticals is a move in the right direction – but for the greatest protection against diabetes, a non-SOS WFPD has been shown repeatedly in additional research studies 29 30   to trump the more watered-down veggie versions.


References

  1. Vegetarian Diets and the Risk of Diabetes. Olfert MD, Wattick RA. Curr Diab Rep. 2018 Sep 18;18(11):101. doi: 10.1007/s11892-018-1070-9. Review. [] []
  2. Cho N, Shaw J, Karuranga S, et al. IDF Diabetes Atlas: global
    estimates of diabetes prevalence for 2017 and projections for 2045. Diabetes Res Clin Pract. 2018;138:271–81. []
  3. Trapp CB, Barnard ND. Usefulness of vegetarian and vegan diets for treating type 2 diabetes. Curr Diab Rep. 2010;10:152–8. [] [] []
  4. McEvoy CT, Temple N, Woodside JV. Vegetarian diets, low-meat diets and health: a review. Public Health Nutr. 2012;15(12):2287–94. []
  5. Snowdon DA, Phillips RL. Does a vegetarian diet reduce the occurrence of diabetes? Am J Public Health. 1985;75(5):507–12. []
  6. Vang A, Singh PN, Lee JW, Haddad EH, Brinegar CH. Meats, processed meats, obesity, weight gain and occurrence of diabetes among adults: findings from adventist health studies. Ann Nutr Metab. 2008;52(2):96–104. []
  7. Fung TT, Schulze M, Manson JE, Willett WC, Hu FB. Dietary patterns, meat intake, and the risk of type 2 diabetes in women. Arch Intern Med. 2004;164(20):2235–40. []
  8. Barnard ND, Katcher HI, Jenkins DJ, Cohen J, Turner-McGrievy. Vegetarian and vegan diets in type 2 diabetes management. Nutr Rev. 2009;67(5):255–63. []
  9. Chen Z, Zuurmond MG, van der Schaft N, Nano J, Wijnhoven HAH, Ikram MA, et al. Plant versus animal based diets and insulin resistance, prediabetes and type 2 diabetes: the Rotterdam Study. Eur J Epidemiol. 2018. []
  10. Yokoyama Y, Barnard ND, Levin SM, Watanabe M. Vegetarian diets and glycemic control in diabetes: a systematic review and meta-analysis. Cardiovasc Diagn Ther. 2014;4(5):373–82. []
  11. Slavícek J, Kittnar O, Fraser GE, et al. Lifestyle decreases risk factors for cardiovascular diseases. Cent Eur J Public Health. 2008;16(4):161–4. []
  12. Crowe FL, Appleby PN, Travis RC, Key TJ. Risk of hospitalization or death from ischemic heart disease among British vegetarians and nonvegetarians: results from the ePIC-Oxford cohort study. Am J Clin Nutr. 2013;97(3):597–603. []
  13. Bunner AE, Wells CL, Gonzales J, Agarwal U, Bayat E, Barnard ND. A dietary intervention for chronic diabetic neuropathy pain: a randomized controlled pilot study. Nutr Diabetes. 2015;5(5):e158. []
  14. What is neuropathic pain? Wikipedia. []
  15. Barsotti G, Navalesi R, Giampietro O, et al. Effects of a vegetarian, supplemented diet on renal function, proteinuria, and glucose metabolism in patients with ‘overt’ diabetic nephropathy and renal insufficiency. Contrib Nephrol. 1988;65:87–94. []
  16. What is diabetic neuropathy? Mayo Clinic. []
  17. What is creatinine and creatinine clearance? WedMD []
  18. Chiu THT, Pan W-H, Lin M-N, Lin C-L. Vegetarian diet, change in dietary patterns, and diabetes risk: a prospective study. Nutr Diabetes. 2018;8:12. []
  19. Nicholson AS, Sklar M, Barnard ND, Gore S, Sullivan R, Browning S. Toward improved management of NIDDM: a randomized, controlled, pilot intervention using a lowfat, vegetarian diet. Prev Med. 1999;29:87–91. []
  20. Turner-McGrievy GM, Barnard ND, Scialli AR. A two-year randomized weight loss trial comparing a vegan diet to a more moderate low-fat diet. Obesity (SilverSpring). 2007;15:2276–81. []
  21. Kahleova H, Matoulek M, Malinska H, et al. Vegetarian diet improves insulin resistance and oxidative stress markers more than conventional diet in subjects with type 2 diabetes. Diabet Med. 2010;28:549–59. []
  22. Anderson JW, Ward K. High-carbohydrate, high-fiber diets for insulin-treated men with diabetes mellitus. Am J Clin Nutr. 1979;32(11):2312–21. []
  23. Barnard RJ, Jung T, Inkeles SB. Diet and exercise in the treatment of NIDDM. The need for early emphasis. Diabetes Care. 1994;17: 1469–72. []
  24. Barnard ND, Cohen J, Jenkins DJ, et al. A low-fat vegan diet improves glycemic control and cardiovascular risk factors in a randomized clinical trial in individuals with type 2 diabetes. Diabetes Care. 2006;29(8):1777–83. []
  25. Tonstad S, Butler T, Yan R, Fraser GE. Type of vegetarian diet, body weight, and prevalence of type 2 diabetes. Diabetes Care. 2009;32(5):791–6. []
  26. Kahleova H, Hrachovinova T, Hill M, Pelikanova T. Vegetarian diet in type 2 diabetes – improvement in quality of life, mood and eating behaviour. Diabet Med. 2013;30(1):127–9. []
  27. Satija A, Bhupathiraju SN, Rimm EB, et al. Plant-based dietary patterns and incidence of type 2 diabetes in US men and women: results from three prospective cohort studies. PLoS Med. 2016;13(6):e1002039. [] []
  28. The Green Room []
  29. Current Diabetes Treatment – Practice or Malpractice? []
  30. Plant-based Diets & Diabetes []

Harvard Study – One Third of Early Deaths Avoided if We Gave Up Meat

Sarah Knapton, Science Editor of the Telegraph reported on the Harvard Study which considers that at least one-third of early deaths could be prevented if everyone moved to a vegetarian diet (not even a WFPBD). The following is a summary of the article1 entitled “Third of early deaths could be prevented by everyone giving up meat, Harvard study finds” in the Science section of the Telegraph 26 APRIL 2018.

Dr Walter Willett, professor of epidemiology and nutrition at Harvard Medical School, speaking at the Fourth International Vatican Conference, Unite to Cure: A Global Health Care Initiative said: (( The Fourth International Vatican Conference, Unite to Cure: A Global Health Care Initiative )) “We have just been doing some calculations looking at the question of how much could we reduce mortality shifting towards a healthy, more plant based diet, not necessarily totally vegan, and our estimates are about one third of deaths could be prevented.  That’s not even talking about physical activity or not smoking, and that’s all deaths, not just cancer deaths. That’s probably an underestimate as well as that doesn’t take into account the fact that obesity is important and we control for obesity. When we start to look at it we see that healthy diet is related to a lower risk of almost everything that we look at. Perhaps not too surprising because everything in the body is connected by the same underlying processes.

Recent figures from the Office for National Statistics (( Office for National statistics: Statistical bulletin: Deaths registered in England and Wales (Series DR): 2013 )) suggested that around 24 per cent or 141,000 deaths each year in Britain were preventable, but most of that was due to smoking, alcohol or obesity.  But the new figures from Harvard suggest that at least 200,000 lives could be saved each year if people cut meat from their diets.

Also speaking at the conference, Dr Neal Barnard 2  said that people need to wake up to the health benefits of vegetarianism and veganism. He continued: “I think people imagine that a healthy diet has only a modest effect and a vegetarian diet might help you lose a little bit of weight. But when these diets are properly constructed I think they are enormously powerful…A low-fat vegan diet is better than any other diet I have ever seen for improving diabetes…With regards to inflammatory diseases like rheumatoid arthritis we are seeing tremendous potential there too. Partly because of things we are avoiding and cholesterol but also because of the magical things that are in vegetables and fruits which just aren’t in spam.

British-born Professor David Jenkins3 , of the University of Toronto, who is credited with developing the glycaemic index 4 also told the conference that the benefits of vegetarianism had been ‘undersold.’  Dr Jenkins said humans would do better following a “simian” diet, similar to lowland gorillas who eat stems, leaves, vines and fruits rather than a “paleo” or caveman diet, which cuts carbohydrates but allows meat.

His team recently teamed up with The Bronx Zoo in New York and travelled to central Africa to record the feeding habits of gorillas.  When they recreated the diet for humans – which amounted to 63 servings of fruit and vegetables a day – they found a 35 per cent fall in cholesterol, in just two weeks, the equivalent of taking statins.  Around 17.5 million people eligible for statins to stave off heart disease, equating to most men over 60 and most women over 65. But many complain of side effects and stop taking the drugs.  Dr Jenkins added: “We’re saying you’ve got a choice, you can change your diet to therapeutically meaningful change or you can take a statin. Drug or diet.”

  1. Third of early deaths could be prevented by everyone giving up meat, Harvard study finds []
  2. Dr Neal Barnard. Physician’s Committee for Responsible Medicine. []
  3. David J Jenkins. Wikipedia. []
  4. Am J Clin Nutr. 1981 Mar;34(3):362-6. Glycemic index of foods: a physiological basis for carbohydrate exchange. Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM, Bowling AC, Newman HC, Jenkins AL, Goff DV. []

Health = Nutrient Intake ÷ Calories

Dr Joel Fuhrman reverses many chronic diseases – not with medications, radiotherapy or invasive surgical procedures like stents, angioplasty or gastric bands – but simply through changing his patients’ diets.

He created the Nutritarian diet, an eating plan that incorporates the latest advances in nutritional science. At the heart of this diet is the simple health equation, H=N/C.

This equation expresses the concept that your health (H) is predicted by your nutrient intake (N) divided by your calorie intake (C). His ANDI (Aggregate Nutrient Density Index) scoring system, which measures the relative nutrient density of common foods, has helped millions of people to eat an anti-cancer, anti-chronic disease diet.

The aim is to get as high a score as possible. Each food has a given value of between 0 and 1000 per calorie.

Examples

(Refer to chart below for individual food values.)

If you eat 300 calories of food with low nutritional value (let’s say 100 calories each of white pasta, cheddar cheese and olive oil), as you will see from the chart below, these would have individual ANDI values per calorie of 11, 11 and 10 respectively. Add these together and you get 32. Multiplying by 100 calories (the amount of each consumed) gives 3200. Divide this by 300 (the total number of calories) and you get a total ANDI score of  10.7.

If, however, you eat 300 calories of food with high nutritional value (let’s say 100 calories each of sweet potato, tomato and kale), these would have individual ANDI values per calorie of 181, 186 and 1000 respectively. Add these together and you get 1367. Multiplying by 100 calories (the amount of each consumed) gives 136700. Divide this by 300 and you get a total ANDI score of 455.7.

Basically, the higher the score, the healthier the food.

What does ANDI measure?

ANDI measures calcium; the carotenoids – beta carotene, alpha carotene, lutein, zeaxanthin, and lycopene; fibre; folate; glucosinolates; iron; magnesium; niacin; selenium; vitamins B1 (thiamine),  B2 (riboflavin), B6, B12, C, and E; and zinc, plus the ORAC (oxygen radical absorbance capacity) score X 2. Most importantly, the ANDI scores are based on calories, not volume or weight of food, so a lower-calorie food with more nutrients scores higher than a calorie-dense food, which is why foods like iceberg lettuce and kale score high.

Have a look below and see how popular foods stack up in terms of micronutrient density per calorie. The more nutrient-dense food you consume, the more you will be satisfied with fewer calories.

So can diet really reverse diseases? And if so which diseases?

The following are some testimonials from Dr. Fuhrman’s patients. (Full TED Talk video covering the issues in this blog can be viewed below.)

Obesity, rheumatoid arthritis, hypertension, cholesterolemia.

Migraines, seasonal allergies, depression, anxiety, insomnia, menstrual pains.

Fibromyalgia, diabetes, hypertension.

Heart disease (no longer needed angioplasty), cholesterolemia, hypertension, obesity.

Psoriatic arthritis, psoriasis.

Triple vessel heart disease, (no longer needed stent replacement & angioplasty), hypertension.

HIPPOCRATES
Let food by thy medicine and let medicine be thy food.

G-BOMBS

Dr. Fuhrman coined the acronym G-BOMBS (Green Beans Onions Mushrooms Berries & Seeds) to represent those foods he considers are the immune system’s “special forces” – inhibiting fat storage, preventing cancer and prolonging our healthy lifespan.

I hope you are able to use this information to enjoy a diet that has food fighting for you rather than against you. After all, we are the food we eat – quite literally…

TED Talk Video


About Dr. Fuhrman

Joel Fuhrman, M.D. is a board-certified family physician, six-time New York Times best-selling author and internationally recognised expert on nutrition and natural healing.

He specialises in preventing and reversing disease through nutritional methods. He coined the term “Nutritarian” to describe his eating style, which is built around a diet of nutrient-dense, plant-rich foods.

For over 25 years, Dr. Fuhrman has shown that it is possible to achieve sustainable weight loss and reverse heart disease, diabetes and many other illnesses using smart nutrition. In his medical practice, and through his books and television specials, he continues to bring this life-saving message to hundreds of thousands of people around the world.

Dr. Fuhrman is the President of the Nutritional Research Foundation. He is also a member of the Dr. Oz Show Medical Advisory Board. He is a graduate of the University of Pennsylvania (Pearlman) School of Medicine (1988) and has received the St. Joseph’s Family Practice Resident’s Teaching Award for his contribution to the education of residents.


References

Dr. Fuhrman’s TED Talk (from which slides were taken)

Dr. Fuhrman’s ANDI scores

Dr. Fuhrman’s website

Chalkboard (more on the ANDI system)

Books:

The End of Diabetes

Super Immunity

Eat Right America

Eat For Health

 

 

 

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.

Definitions

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…

 

 


Glossary

  1. ” Of or pertaining to honey” – https://en.wiktionary.org/wiki/mellitus.
  2. “The physiological processes associated with disease or injury” – https://en.wiktionary.org/wiki/pathophysiology
  3. “The metabolic process in which glucose is formed, mostly in the liver, from non-carbohydrate precursors” – https://en.wiktionary.org/wiki/gluconeogenesis
  4. “The presence of sugars (especially glucose) in the urine, often as a result of diabetes mellitus” – https://en.wiktionary.org/wiki/glycosuria
  5.  “The production of an abnormally large amount of urine; one symptom of diabetes” – https://en.wiktionary.org/wiki/polyuria
  6. “Any of several compounds that are intermediates in the metabolism of fatty acids” – https://en.wiktionary.org/wiki/ketone_body#English.
  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” – https://en.wiktionary.org/wiki/ketosis.
  8. “A severe form of ketosis, most commonly seen in diabetics, in which so much ketone is produced that acidosis occurs” – https://en.wiktionary.org/wiki/ketoacidosis.
  9. “A state of decreased blood volume” – https://en.wiktionary.org/wiki/hypovolemia#English.
  10. “An abnormally low concentration of sodium (or salt) in blood plasma” – https://en.wiktionary.org/wiki/hyponatremia#English.
  11. “The condition of having an abnormally low concentration of potassium ions in the blood” – https://en.wiktionary.org/wiki/hypokalemia#English.
  12. Angiopathy of the larger blood vessels” – https://en.wiktionary.org/wiki/macroangiopathy.
  13. Angiopathy of the small blood vessels” – https://en.wiktionary.org/wiki/microangiopathy.
  14. “Non-inflammatory disease of the retina” – https://en.wiktionary.org/wiki/retinopathy.
  15.  “Damage to, disease of, or abnormality of the kidneys” – https://en.wiktionary.org/wiki/nephropathy.
  16. “Any disease of the peripheral nervous system” – https://en.wiktionary.org/wiki/neuropathy.
  17. “A fungal infection of any of the Candida (yeast) species” – https://en.wiktionary.org/wiki/candidiasis. Also called “thrush”.
  18. “An ascending urinary tract infection that has reached the pelvis of the kidney” – https://en.wiktionary.org/wiki/pyelonephritis.

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.