Type 2 Diabetes Can Be Reversed

The title may appear medical heresy but it is absolutely true, and the only thing you can be sure of is that modern medicine and the pharmaceutical industry don’t want you to know this is the case.

A health professional will tell you:
“Type 2 diabetes mellitus is a progressive chronic disease that frequently results in amputation, kidney disease, heart disease, blindness, and premature death. Treatment is focussed on blood sugar control and reduction of these complications.”

Diabetes mellitus has for many decades been described as disease of sugar metabolism. The lay explanation is: “Glucose needs insulin in order to enter the cells to be used as energy. When people get fat and unfit, their body does not respond to insulin very efficiently any more, so the pancreas has to pump out more insulin to do the same job. Eventually the pancreas becomes so overworked that it stops producing enough insulin to keep blood glucose within the normal range – viola, you now have diabetes.”

Type 2 diabetes is also described as a ‘lifestyle disease’, which suggests those suffering the dreaded condition brought it on themselves. Somehow, if they had listened to the ‘experts’, this would not have happened. The lay public, and science and medicine accept this without question and without logic.
The most common misconceptions are:
Too many calories in plus not enough exercise equals weight gain
Insulin resistance is the result of weight gain and poor exercise habits

In other words, people get diabetes because they are greedy, fat and lazy.

As in so many other erroneous medical theories, science has put the cart before the horse.

If being fat causes diabetes then why don’t all fat people have diabetes?
Why do thin people get diabetes?
Why do many people (fat or thin) get diabetes even though they get plenty of exercise?

At this point science will probably offer “genetics” as an explanation. However, diabetes prevalence and incidence has increased at a far greater rate than can be explained by inheritance of dodgy genes.

Diabetes 101

The primary mechanism in diabetes is not impairment in glucose metabolism, but impairment of fatty acid oxidation [1, 2]. The high blood glucose is only a downstream effect (a symptom) of diabetes and not the disease itself. While a symptom is the only aspect addressed by medicine, of course it can never be ‘cured’.
To add insult to medical injury, the interventions used in the treatment of diabetes make the underlying problem worse.

In a normal healthy person the little energy furnaces in the cells, known as the mitochondria, burn both fatty acids and glucose (carbohydrates). On rising in the morning (assuming you are not a shift worker) there is not much spare glucose left in the blood, so the cells (apart from the brain) will be burning fatty acids. At this point you are temporarily insulin resistant. When a high carbohydrate cereal or toast breakfast is eaten the blood sugar rises rather rapidly, insulin is released (because the blood glucose has to be kept to a narrow range) and the cells then switch to burning glucose. This metabolic switch involves many enzymes and proteins and is very complex. However, the concept that the flexibility of the switch determines the likelihood of diabetes could not be simpler – this metabolic inflexibility is termed mitochondrial dysfunction. It is this dysfunction that leads to chronic insulin resistance that may result in fatness (not obligatory) and diabetes [3].


Medical treatment has always focussed on blood glucose and glycosylated haemoglobin (a longer term measure of blood glucose control) and has (until recently) blithely ignored the primary problem. Every current mainstream intervention is counter-intuitive and leads to an increased disease burden.

Intervention 1 – Diet

People with diabetes are advised to eat a high carbohydrate, low fat diet. More carbohydrate means a higher requirement for insulin. Because the pancreas has a finite insulin producing capacity, this speeds up total pancreatic exhaustion.

Much of the damage to the heart, kidneys, nerves and the retina of the eye occurs before blood sugar levels are high (prediabetes) and these effects are initiated by high circulating insulin levels.

While tissues can become resistant to insulin’s glucose handling effects, they do not become resistant to its effects on growth and cell differentiation that predisposes to certain cancers, heart muscle remodelling (heart failure), inflammation, atherosclerosis, and liver damage. Nor are fat cells immune to this growth effect; insulin causes preadipocytes (fat stem cells) to grow into fully-fledged fat cells [4], and incidentally, vitamin D has the opposite effect [5].

Lipoprotein lipase (LPL) is a little-known but extremely important enzyme involved in fat metabolism. A basic understanding of its actions is necessary to explain why a high carbohydrate diet makes no sense.

The very low-density lipoprotein (VLDL) and chylomicrons (both elements of the total cholesterol measurement) are the ‘taxis’ that shuttle triglycerides (three fatty acids attached to a glycerol backbone) around the body. LPL is the enzyme that enables the fatty acids on triglycerides to detach themselves into fat cells for storage, and into other tissues to be used for energy.

Insulin increases LPL activity in fat tissue, but decreases it in skeletal muscle [6, 7]. Heart muscle cells derive most of their energy from lipoprotein-bound fatty acids [8] making LPL activity in the heart crucial. The heart muscle cells prefer to burn fatty acids for energy [9] and saturated ones at that [8]. When heart muscle cells have to burn predominantly glucose for energy over the long term, the heart becomes impaired [10]. Decreased fatty acid oxidation in the heart might be a good thing in an acute setting when you are just about to have a heart attack (it’s called ischaemic preconditioning) but it’s a terrible idea over the long term. One research paper concluded “our studies demonstrate that the heart has an optimal balance between use of glucose and FA [fatty acids]. Chronically altering this balance may lead to cardiac dysfunction” [10]. Is it any wonder why heart disease is so common in diabetes?

While insulin is high the body favours fat storage over fat burning. High insulin and high glucose together decreases LPL activity by 44% [11]. Glucose decreases and inactivates LPL [12, 13] and high blood glucose alone can decrease LPL by 40% [11]

LPL activity differs between the sexes; fat cell size in females correlates with LPL activity in thigh, gluteal and abdomen, but in males this was seen only in the abdomen [14]. Now you know why men put most excess fat on their abdomen (beer-belly) and women on their abdomen, thighs and bottom.

The end result of all this LPL depression is going to be weight gain, heart problems and further loss of metabolic flexibility (mitochondrial dysfunction).


Calorie counting is another rather useless tool in the diabetes control armoury. The idea that ‘a calorie is a calorie is a calorie’ is ridiculous:
a) We are not simple bomb calorimeters (method used to measure a ‘calorie’) and the use of this simple device to somehow determine what ‘calorie intake’ is necessary in human beings (of various shapes and sizes, with various energy outputs) has a ‘flat earth’ dimension.
b) The final destination of what we eat is not exactly straightforward. Most protein is used to replace worn out body parts or to make enzymes so I’m doubtful it should even figure in calorie counts because it is rarely used for direct energy requirements.

Starchy fibre supposedly provides 4 calories per gram. What isn’t so well known is that when fibrous starch gets into the large intestine, gut bacteria will break it down and the by-product of all this bug munching activity is FAT, which then gets absorbed directly by the intestine and may provide as much as 10% of total daily energy intake (an extra large chocolate bar per day!) [15].
The USDA recommendation to consume six to eleven servings of starch per day sounds more like a recipe for blimpdom than for healthy eating. This level of carbohydrate will speed you into diabetes and weight gain in no time.

Intervention 2 – Sulphonylurea (hypoglycaemic) drugs and more recent insulin secretagogues

Sulphonylurea and more recent secretagogue drugs stimulate the pancreas to produce more insulin, which again speeds up total pancreatic exhaustion. Unfortunately the sulphonylureas’ mechanism of action on the pancreas also has a detrimental effect on the heart leading to a doubling of heart attack risk [16]. The more recent secretagogues may not have this effect on the heart, but still hasten pancreatic exhaustion.


Once pancreatic exhaustion occurs injected insulin will be advised.

Intervention 3 – PPAR-gamma agonists - thiazolidinediones (TZDs)

These drugs are supposed to decrease insulin resistance by redistributing the way fat is stored throughout the body. They promote weight gain, further impair fatty acid oxidation and can cause heart failure [10].
Insulin resistance does not just occur in skeletal muscle, but in cardiac muscle as well. PPAR-alpha is expressed mostly in the liver, renal cortex, intestine and heart, and PPAR-gamma is expressed mainly in smooth muscle cells in blood vessels, immune cells and white adipose tissue [17].
Because TZDs are PPAR-gamma agonists, they may improve “whole body” insulin resistance, but they leave cardiac tissue resistant and unable to utilise glucose for oxidation during ischaemia. That these terribly clever scientists profess not to know how these agents cause heart failure is nothing short of bizarre.
PPARgamma agonists promote fat storage rather than fat oxidation. Not only is the heart being deprived of its preferred energy source – fatty acids, it is also being deprived of its secondary source thanks to myocardial insulin resistance. A heart running on suboptimal levels of energy is going to suffer.


Intervention 4 – Insulin

Apart from the above described deleterious effects on the body, insulin promotes fat storage leading to weight gain [18] leading to increased insulin resistance leading to increased insulin dosage leading to further weight gain…you get the picture, until the insulin dose you need to control blood glucose would stop a charging bull elephant in its tracks.

Other interventions: Antihypertensive medications, statins and weight loss drugs.

Many people with diabetes also have high blood pressure. Some of the treatments used make blood glucose control even trickier and can even induce diabetes in people who didn’t have it to start with.

Statins (HMG-CoA reductase inhibitors) are increasingly prescribed in patients with diabetes to lower cholesterol even when it isn’t particularly high. These drugs can have life-threatening side effects and have been associated with an increased risk of heart failure. The mechanism of action for lowering cholesterol also lowers levels of Coenzyme Q10; a substance that is already deficient in patients with diabetes [19]. This further exacerbates mitochondrial dysfunction.

Xenical (orlistat) prevents fat absorption from the intestines, but it also prevents the absorption of fat-soluble vitamins. Loss of antioxidant function from vitamins worsens mitochondrial dysfunction.

Meridia (sibutramine) produces only modest weight loss, but increases blood pressure. While it does not appear to have the rare but fatal side effect, primary pulmonary hypertension, I think caution is warranted with any drug that acts directly on the nervous system.

All the interventions employed in the battle with type 2 diabetes further aggravate the underlying problem of mitochondrial dysfunction and increase the likelihood of weight gain, heart problems and other diabetic complications. Why don’t scientists and doctors admit their current approach is nonsensical, unethical and deadly? The phrase “the treatment was a success but the patient died” certainly springs to mind. They were trained to treat the symptoms – high glucose, high cholesterol etc. by the very industry that profits so much from diabetes. They were not schooled in nutrition or preventative medicine. Theirs is a reactive rather than proactive model and the only weapons in their armoury are drugs and radical surgery. The dietary dogma that has unjustly framed saturated fat and promoted refined carbohydrate as healthy remains firmly entrenched in their psyche and it doesn’t look likely to change any time soon.

As long as there is some residual pancreas function, type 2 diabetes is reversible. Even if very little function remains, it makes absolute sense to reduce the requirements for insulin. Diabetes is a nutritionally induced disease and the only way to beat it is to use primarily nutritional means.

When the outdated ‘refined vs unrefined carbohydrate’ theory was finally shown the door, nutritionists and diet book writers embraced the Glycaemic Index (GI). The GI is a measure of how fast something you eat increases your blood sugar. When it was revealed that potatoes had the same GI as table sugar, the ADA responded by advising people with diabetes that it was now considered okay for them to eat table sugar!
This highlighted just how ignorant the ADA is in relation to nutrition. They completely ignored many other issues:
Sugar is half glucose and half fructose. Fructose has very different metabolic consequences than does glucose. Potatoes break down into glucose and do at least contain some Vitamin C. It is the effects of large amounts of fructose and sugar generally, consumed regularly in the Western diet that poses such a problem.
The GI measures foods in isolation and people rarely eat from one single food group. Adding butter to potato reduces its GI considerably.

The full horror of fructose is the subject of a future article, but for the purposes of an article on diabetes it is important to know that fructose suppresses PPAR-alpha in the liver (alpha promotes fat burning)[20], while too much glucose activates PPAR-gamma (promotes fat storage) [21]. A high carbohydrate diet – especially one containing chemical fructose is one that promotes weight gain and worsens fatty acid oxidation – obviously the last thing you want to do, especially in diabetes.


So the six million dollar question is…how exactly does one ‘reverse diabetes’?

Find a physician or ND familiar with low carbohydrate diets and work closely with him/her to lower (and eventually abolish) the need for medications without putting you at risk of hypo- or hyperglycaemia. He/she will also need to assist you with getting the omega-3:omega-6 fatty acid ratio corrected (very important), and to advise on supplements to offset some of the metabolic imbalances.


Consume only FRESH WHOLE FOODS, preferably organic, in as close to their natural state as possible. Eat nothing processed, including sugar, anything sweetened with high fructose corn syrup, MSG, aspartame, other assorted additives, refined vegetable oils and trans fats. Any confusion as to whether something is processed can be dispelled by the question “did my ancestors eat this hundreds of years ago?”

Cut right back on the carbohydrates (including high-sugar fruit) and eat natural fats like butter and coconut oil. For anyone that still believes that saturated fat is deadly, I recommend you read Dr Mary Enig and Sally Fallon’s brilliant article on saturated fat here.

Exercise moderately (not vigorously) at least ½ - 1 hour, three to five times per week. Moderate exercise can include cooking, housework, swimming, resistance training, walking and gardening – you don’t need an expensive gym membership.

Things known to improve mitochondrial function:
Exercise
R-Alpha Lipoic Acid
N-Acetyl Cysteine
Omega-3 fatty acids
Carnitine
Coenzyme Q10
Magnesium
Glutathione
B vitamins (1,2,3)
Vitamin C
Vitamin E
Vitamin K
EDTA
D-ribose
Creatine
Taurine
Ginko Biloba

1. Befroy, D.E., et al., Impaired mitochondrial substrate oxidation in muscle of insulin-resistant offspring of type 2 diabetic patients. Diabetes, 2007. 56(5): p. 1376-81.
2. Kelley, D.E., et al., Skeletal muscle fatty acid metabolism in association with insulin resistance, obesity, and weight loss. Am J Physiol, 1999. 277(6 Pt 1): p. E1130-41.
3. Duchen, M.R., Roles of mitochondria in health and disease. Diabetes, 2004. 53 Suppl 1: p. S96-102.
4. Pekala, P.H., et al., On the mechanism of preadipocyte differentiation. Masking of poly(ADP-ribose) synthetase activity during differentiation of 3T3-L1 preadipocytes. J Biol Chem, 1981. 256(10): p. 4871-6.
5. Zhuang, H., Y. Lin, and G. Yang, Effects of 1,25-dihydroxyvitamin D(3) on proliferation and differentiation of porcine preadipocyte in vitro. Chem Biol Interact, 2007.
6. Lithell, H., et al., Lipoprotein-lipase activity in human skeletal muscle and adipose tissue in the fasting and the fed states. Atherosclerosis, 1978. 30(1): p. 89-94.
7. Lithell, H., et al., Is muscle lipoprotein lipase inactivated by ordinary amounts of dietary carbohydrates? Hum Nutr Clin Nutr, 1985. 39(4): p. 289-95.
8. Ballard, F.B., et al., Myocardial metabolism of fatty acids. J Clin Invest, 1960. 39: p. 717-23.
9. van der Vusse, G.J., et al., Fatty acid homeostasis in the normoxic and ischemic heart. Physiol Rev, 1992. 72(4): p. 881-940.
10. Augustus, A.S., et al., Loss of lipoprotein lipase-derived fatty acids leads to increased cardiac glucose metabolism and heart dysfunction. J Biol Chem, 2006. 281(13): p. 8716-23.
11. Kovar, J., et al., Hyperglycemia downregulates total lipoprotein lipase activity in humans. Physiol Res, 2004. 53(1): p. 61-8.
12. Jindrichova, E., S. Kratochvilova, and J. Kovar, Glucose administration downregulates lipoprotein lipase activity in vivo: a study using repeated intravenous fat tolerance test. Physiol Res, 2007. 56(2): p. 175-81.
13. Wu, G., et al., A transcription-dependent mechanism, akin to that in adipose tissue, modulates lipoprotein lipase activity in rat heart. Am J Physiol Endocrinol Metab, 2007.
14. Votruba, S.B. and M.D. Jensen, Sex differences in abdominal, gluteal, and thigh LPL activity. Am J Physiol Endocrinol Metab, 2007. 292(6): p. E1823-8.
15. Bergman, E.N., Energy contributions of volatile fatty acids from the gastrointestinal tract in various species. Physiol Rev, 1990. 70(2): p. 567-90.
16. Bell, D.S., Do sulfonylurea drugs increase the risk of cardiac events? Cmaj, 2006. 174(2): p. 185-6.
17. Rosen, E.D. and B.M. Spiegelman, PPARgamma : a nuclear regulator of metabolism, differentiation, and cell growth. J Biol Chem, 2001. 276(41): p. 37731-4.
18. Holman, R.R., et al., Addition of Biphasic, Prandial, or Basal Insulin to Oral Therapy in Type 2 Diabetes. N Engl J Med, 2007.
19. Lim, S.C., et al., Oxidative burden in prediabetic and diabetic individuals: evidence from plasma coenzyme Q(10). Diabet Med, 2006. 23(12): p. 1344-9.
20. Kelley, G.L. and S. Azhar, Reversal of high dietary fructose-induced PPARalpha suppression by oral administration of lipoxygenase/cyclooxygenase inhibitors. Nutr Metab (Lond), 2005. 2: p. 18.
21. Panchapakesan, U., C.A. Pollock, and X.M. Chen, The effect of high glucose and PPAR-gamma agonists on PPAR-gamma expression and function in HK-2 cells. Am J Physiol Renal Physiol, 2004. 287(3): p. F528-34.

Disclaimer: The information published herein is not intended to be used as a substitute for appropriate care by a qualified health practitioner.

Can calorie restriction really extend lifespan?

Each time the media proclaims “Eat Less and Live Longer” people may ponder the question of whether increasing their health and lifespan by reducing calories is a good option. Is eighty more years of daily rabbit food-fuelled misery a good trade off for fifty years of dietary delight (with a possible few miserable ones at the end)?
Well this agonising choice may be unnecessary thanks to our friends at big Pharma.
There are novel therapeutic compounds in the pipeline that could mean you don’t have to forego that pastry after all.

Amid much Shylock-like hand rubbing and Porsche catalogue perusing, the scientists are wetting their proverbial Armani underpants at the prospect having created a highly lucrative magic pill that will simulate calorie restriction and exercise – without having to deny yourself a single morsel or getting off your pizza-encrumbed comfy chair. It’s called SRT501 and it’s already in Phase 2 clinical trials in patients with type 2 diabetes.

Should we just accept that calorie restriction or its pharmaceutical equivalents increase health and longevity at face value?

I would like to mention some reasons why we shouldn’t.

All the studies conducted thus far have involved only laboratory animals. This research needs to be taken with a pinch of low-calorie salt because extrapolating animal studies to humans is particularly problematic in this instance.

Rodents in the laboratory hardly simulate human real life. Rats don’t have to pry themselves out of bed in the morning, negotiate rush hour traffic and spend 8+ hours dealing with irritating customers, lazy colleagues or ogre bosses. They don’t return after a gruelling day to a house full of noisy, selfish teenagers, patronising, bossy mother in laws or screaming colicky infants. No, they laze about in their cages contemplating their navels.

Rats and mice fed fewer calories do appear to live longer - but don’t step away from the donut just yet. Rat chow is the standard laboratory diet in these studies, and judging by its composition, living longer would not be a welcome prospect; if these animals could talk they would plead to be euthanised.

Most of the energy provision in rat chow is from processed cornstarch; it has a high glycaemic index, is anti-thyroid and promotes weight gain – not exactly a health food and certainly not a natural diet for a rat. So the less calories angle could easily be interpreted as ‘feeding less crap food to rats promotes longer life’.

Glucose metabolism in rodents is different to human glucose metabolism. This difference is allegedly why the compound alloxan (it’s added to our flour) produces diabetes in these hapless furry creatures but apparently leaves our own pancreatic beta cells relatively unscathed.
There have been cell studies in human tissue in test tubes, but that doesn’t convincingly simulate real life either. To be convincing (to me at any rate), large-scale human trials need to be conducted in age-, socio-economic status-, rotten boss-, traffic conditions-, unruly teenagers-, baby-shrieking-, unreasonable mother-in-law-matched subjects who would be randomised to eat a normal diet or a calorie restricted one, and followed up for over 50 years to analyse which group lived the longest and healthiest.

The ‘fountain of life’ enzymes in the body that fasting (and the magic pill) induce are called sirtuins. These sirtuins rejuvenate the mitochondria (little energy burning furnaces) in every cell allowing them to be more efficient and long-lived. Not a great deal is known about these enzymes apart from the possibility of generating vast amounts of revenue because they have only recently been discovered.
SIRT1 is necessary in the fasted state (lower blood glucose) to allow the mitochondria to switch from burning glucose to burning fatty acids as fuel. So in conditions of low blood glucose, sirtuin-1 is increased. The magic pill SRT501 increases sirtuin-3 and sirtuin-4. SIRT3 is responsible for protecting the mitochondria during cellular stress and in brown fat it increases thermogenesis [1], theoretically contributing to the armchair-assisted weight loss. SIRT4 produces an insulin-degrading enzyme and depletion leads to a greater insulin response to glucose [2, 3].

So it appears that the sirtuins are an integral mechanism in insulin response (but there are many others; nothing in physiology is that simple). Insulin at low levels is necessary for life, but at continually high levels (as we have with Western diet) it is extremely damaging. The take-home message could then be “eat less crap and live longer” rather than the simple “eat less – period”.

All the enzymes, hormones, minerals, proteins and lots of other factors in the human body are regulated by a complex loop-feedback mechanism (this is why so little of the brain is concerned with conscious thought – regulation of the body needs a lot of brain power). They are finely tuned on a moment-by-moment basis to do their respective jobs; too little or too much either way and you may find you are suffering a horrible disease or have even dropped dead on the spot. Increasing or blocking the actions of these substances with synthetic molecules that override this fine-tuning is a recipe for disaster. Notable molecule-meddling tragedies include Vioxx, thalidomide and several diabetes drugs. When scientists find a substance in the body with a ‘good’ action they want to increase it because they figure more is better. The converse is also true. But the fact is they haven’t fully explored what other actions the substance has. Vioxx caused an increase in heart attacks is because it blocked COX-2, an enzyme involved with inflammation. They decided COX-2 was bad so it had to be stopped at all costs. What they hadn’t bothered to discover was that COX-2 protected the heart.
Meddling with glucose and fat metabolism can increase the risk of all sorts of nasty diseases - SIRT3 levels are much higher in breast cancer [4]. One review entitled Sirtuins: critical regulators at the crossroads between cancer and aging [5] admitted “By participating in the stress response to genomic insults, sirtuins are thought to protect against cancer, but they are also emerging as direct participants in the growth of some cancers.” Tinkering with your sirtuins sounds like a game of Russian roulette.

Here’s a whacky idea – instead of traipsing down the rabbit food road, or spending the kids’ college funds on an expensive, potentially toxic pill, a cheaper, safer option (well, free actually, unless you want to pay me for this advice) – is to eat…less…carbohydrate – especially sugar.


1. Shi, T., et al., SIRT3, a mitochondrial sirtuin deacetylase, regulates mitochondrial function and thermogenesis in brown adipocytes. J Biol Chem, 2005. 280(14): p. 13560-7.
2. Ahuja, N., et al., Regulation of insulin secretion by SIRT4, a mitochondrial ADP-ribosyltransferase. J Biol Chem, 2007.
3. Haigis, M.C., et al., SIRT4 inhibits glutamate dehydrogenase and opposes the effects of calorie restriction in pancreatic beta cells. Cell, 2006. 126(5): p. 941-54.
4. Ashraf, N., et al., Altered sirtuin expression is associated with node-positive breast cancer. Br J Cancer, 2006. 95(8): p. 1056-61.
5. Saunders, L.R. and E. Verdin, Sirtuins: critical regulators at the crossroads between cancer and aging. Oncogene, 2007. 26(37): p. 5489-504.