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The Safe Keto Diet

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03 Apr 2019 Diets

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The Safe Ketogenic Diet

Ketosis occurs when carbohydrate levels are low enough to suppress insulin activity allowing Hormone Sensitive Lipase (HSL) an enzyme in adipose tissue to now become active and release free fatty acids (FFAs) which can then be burnt off as energy or converted to ketone bodies. Ketone bodies in turn can be an effective energy source for your heart and brain once these organs adapt to the use of these compounds for their energy needs.

"Nothing in Biology Makes Sense Except in the Light of Evolution"

This was the heading of an essay by Prof Theodosius Dobzhansky an emeritus professor at the Rockefeller University and adjunct professor of genetics at the University of California, Davis when in 1973 he published his thoughts in The American Biology Teacher3

We often talk about diets and their benefits but rarely do we place this in the context of evolution and why a mechanism such as the production of ketone bodies conferred an advantage to humans enabling them to survive lengthy spans of famine. 

Our molecular and biochemical cellular  'machinery' developed out of this constant struggle by humanity  to survive food shortages perhaps for long periods or even food shortages with no end in sight where ultimately the end result was death by starvation. Refined or simple carbohydrates being available for consumption by our ancient ancestors in early evolutionary development apart from the rare taste of honey or more commonly wild fruits when seasonally available, would have been uncommon. Early humans were scavengers living off the carcasses of animals killed by other animals as this required far less energy lost in the hunt, and it was also significantly less dangerous.

There was nothing in the ancestral forests or on African Savannahs that came out of a box containing a vast amount of carbohydrate in one serving. For those who think that early man ate wild grass seeds, grasses and sedges, why not try putting wild grass seeds or sedges into a bowl after a tremendous amount of effort to even manually gather wild grass (grain) seeds in sufficient amounts, and then try to eat this unpalatable, indigestible mix perhaps moistened into an uncooked gruel with muddy water. No cow or nut milks available either. If our ancient ancestors did indeed eat difficult to gather grass seeds (cereal grains are grass seeds) or the more plentiful leafy grasses and sedges, these would simply be passed through their bowels undigested. Prior to the harnessing of fire that occurred at the most 1.7 million years ago i.e in an evolutionary 'blink-of-an-eye', eating a raw potato could have had toxic  effects due to glycoalkaloids and any root vegetable would have been indigestible without fire and cooking to break down the cellulose, destroy pathogens and toxins and allow the energy-laden carbohydrates to become available from tubers . The raw grass seeds (grains) or grasses/sedges would be at the least rich in indigestible fibre but the carb content would be markedly low in comparison to grains crushed by industrial compressors and then shaped into flakes or rectangular biscuits or loops and then put into boxes and marketed for their 'health value'. 

The argument that early hominins ate grass seeds is debated as the incorporation of C4 carbon atoms from these plant-based sources in teeth or bones may have come from the flesh and organs of ruminant animals eaten by early ancestors where these animals were able to digest the plants through fermentation in the rumen that converts indigestible plant matter like cellulose to utilizable nutrients that were then incorporated into their animal flesh and organs subsequently consumed by hominins.

However, we need to go much further back in our evolutionary history to a time even before we stepped onto the plains of Africa and back in time to the forests where our ancestors evolved to use C3 carbon sources (trees, shrubs, herbs) and long before a mortar and pestle was ever used to grind grains into flour or fire to access indigestible carbohydrate from grains. It is at this extremely early pre-human hominid time that our molecular mechanisms and cellular biochemistry adapted to the environment and available food sources. These food sources have changed dramatically from post-agricultural practices and post-industrialization. These forests were also subject to fire, plagues of pests, pathogens, competition for food sources and climatic shifts. So even our early forest dwelling ancestors faced the threat of famine.

To survive food shortages, the body needed to evolve a mechanism to use an energy source other than glucose and this was to use body fat stores and ketone bodies when insulin levels in the blood were very low and this happens with a low-carbohydrate intake. 

It is fatuous to think we can adapt rapidly to hamburgers and chips and that there is no cost to humanity in the excruciatingly slow process of evolutionary adaptation. The fact that humans adapted to milk consumption is sometimes thrown up as an amazingly rapid adaptation to dietary change but at what cost? Lactose intolerance leading to chronic and persistent diarrhoea, abdominal gas and colicky pain associated with malabsorption thus leading to muscle weakness, lethargy, anaemia along with osteomalacia and osteoporosis causing painful bony complications that include crush fractures of the spine and limb deformities meant that millions would have perished in abject misery allowing Darwinian processes to eliminate the weak and pass on the genetic ability to digest milk through production of the enzyme lactase. Milking large and dangerous Auroch cattle would have been an act of desperation in a time of famine - an act of survival.  

So early man was always under threat of starvation and without a constant supply of glucose, insulin levels would have been markedly lower than in modern man. Today we live in a time of perennial plenty due to mighty agricultural and industrial machines and the constant high-energy snacking and high carb modern meals mean insulin levels are constantly driven upwards thus ensuring fat and ketone bodies are not used as a fuel supply. The body just doesn't need to tap into stored body fat due to a never ending supply of glucose from carbs.

Who will benefit from a Ketogenic Diet?

  1. Those with chronic diseases such as heart disease, hypertension, prediabetes, diabetes, early dementia, inflammatory disorders
  2. Those overweight or obese as insulin and leptin sensitivity are improved
  3. Anyone with deep visceral fat and this may be someone who appears to be lean - The TOFI's (Thin on the Outside and Fat on the Inside)
  4. Those concerned about cancer as this type of diet will dampen down the Insulin/IgF-1 axis where high Insulin/IgF-1 levels are a powerful cell multiplication stimulus
  5. Anyone wanting to age well and stay lean and strong

Insulin Resistance & Health Risk

If you have a lot of fat around your belly, then there is a very good chance that you have insulin-resistance which is a prediabetic state.

Around 4 million Australians are prediabetic1 and we can add another 1.2 million people to this tally that are fully-blown diabetics. It has been estimated that around 89 million people in the USA are prediabetic. This means that a huge number of people in Western populations are insulin-resistant with high insulin levels 24/7. It is thought that up to 70% of those with prediabetes (insulin resistance) will go on to develop gross diabetes2. This vast pool of insulin-resistant individuals will find it very hard to lose weight and this includes a significant number of young women with Polycystic Ovarian Syndrome (PCOS).

Anyone with a large waist circumference (abdominal adiposity) should consider themselves insulin-resistant until proven otherwise. This central deposition of toxic fat that you see in so many individuals around their waists is a recipe for disaster as this toxic fat creates a multitude of metabolic shifts that will shorten your life in many ways through chronic disease states that include cancer and dementia.

Inducing ketosis can help to significantly improve these metabolic changes and to decrease this accumulation of deep visceral (toxic) fat around the waist.

The distinction between prediabetes and diabetes is a moot point as the vast majority of research points to the slow and progressive damage done to the cardiovascular system, organ systems and the brain due to the potentially damaging cellular effects of the Insulin/IgF-1 axis and the marked spikes in glucose/insulin in the after-eating (postprandial) period.

These glucose spikes occur with every morsel of food you put in your mouth and with every meal and snack and where these after-eating glucose elevations continually and cumulatively damage every cell and tissue in the body. This is how diabetics suffer so many complications and why we measure a haemoglobin called 'glycated' haemoglobin (HbA1c) in diabetics because when this protein is glycated (damaged by glucose with all the spikes in blood glucose after eating over time), it tells you that all proteins in the body are just as affected in organs such as the kidneys, retina, lens of the eye, proteins in the brain etc. 

The after-eating (postprandial) surges in glucose are tremendously damaging to everyone and a safe ketogenic diet will go a long way towards protecting your body long term from these adverse metabolic effects of eating.

How are ketone bodies produced?

 

What are some of the myths of a ketotic diet?

 

Myth Concern

You can eat as much protein as you like!

Answer: No - The body is not designed for an unlimited supply of any macronutrient or micronutrient. There are many risks inherent in eating a vast amount of protein.

  1. Protein stimulates the mTOR protein synthesis pathway 
  2. Protein can profoundly stimulate insulin release - L-Leucine is a powerful insulin secretagogue and is one of the 9 essential amino acids (EAAs) and a Branched Chain Amino Acid (BCAA). L-Leucine is abundant in animal flesh. 
  3. High intakes of protein have been shown to increase the risk of cancer4. High Insulin/IgF-1 levels are a risk for cancer and low protein intakes decrease IgF-1 a powerful anabolic hormone. 
  4. The more you stimulate anabolic pathways the greater the pressure for cellular multiplication. This is a feast (plenty) response where more fat is stored, muscles become stronger, preparing the body for reproduction and child rearing in times of good and to store energy for the inevitable cycle to turn with famine around the corner. Cell multiplication due to high energy sources available (time of plenty) also occurs in organs and hormone sensitive tissues like the breast and prostate. The more cells multiply, the greater the risk for a genetic error to occur and thus cancer. The other issue is that many studies have shown that abnormal cells already exist in these high-risk hormonal tissues like breast and prostate as we age and thus 'pouring fuel on the fire' is never going to be a great thing - don't poke the bear!
  5. Excess protein can and will be converted to FAT. The mild increase in thermogenesis caused by protein will not offset a substrate abundance that triggers off a far more powerful evolutionary mechanism and that is to conserve energy in the form of energy stores in times of plenty and where fat can store a great deal of energy for one of humanity's most powerful drives - reproduction and child bearing! 
  6. As one of the most highly regarded graphical texts on biochemistry states about protein being converted to fat:

    “In spite of the exhortation by some popular weight-reducing diets to eat large quantities of protein, it should be remembered that surplus dietary protein can be converted to fat. For protein to be converted to fatty acids and triacylglycerols, the essential precursors for fatty acid synthesis, namely a carbon source, acetyl CoA, and biosynthetic reducing power as NADPH, must be formed.” (Salway 2006) Triacylglycerols is another term for triglycerides.

     
  7. Animal flesh seems to be a cardiovascular risk through a compound called TMAO6. Trimethylamine N-oxide (TMAO) is an amine oxide that is generated from choline, betaine, and carnitine in animal flesh through gut microbial metabolism leading to numerous risk factor changes for cardiovascular disease. 

Can you can eat as much fat as you like?

 

Answer: A Definite NO!

  1. Fat has been a precious commodity in our evolution. It is packed with energy and releases far more energy from cellular metabolism than carbohydrate or protein and is found in much higher concentrations in animal flesh than plant sources. 
  2. Even just one high-fat meal can release significant and damaging amounts of Endotoxin or Lipopolysaccharide (LPS) into the bloodstream known as Endotoxemia7
  3. LPS potently increases inflammation in the postprandial (after-eating) phase i.e. the damaging effect that occurs in your body after eating any meal. Initially it was thought that the majority of damage to cells and their organelles after eating was due to the release of free radicals and glycation caused by the elevated levels of glucose due to the carbohydrate component in a meal but we now know that LPS or Endotoxin is a significant contributing factor to after-eating inflammation thus damaging every cell, protein and tissue incrementally and cumulatively over your lifespan. Food is not benign. It is simply an amalgam of chemicals that the body metabolises for energy or to build molecules and tissues. There are inherent dangers to all food consumed 
  4. LPS also potently upregulates atherosclerosis genes7. What this is indicating is that high-fat intakes may be contributing to long-term risk of heart disease and vascular disease. 
  5. A constant high inflammatory process in the body will increase the risk of many cancers, chronic diseases, a worsening of any inflammatory condition whether this is dermatitis or asthma and will risk the development of dementia such as Alzheimer's. Let's face it, when in Western worlds do people stop eating to allow their body to repair and to decrease inflammation? They eat and graze all day thinking that if they miss out on a meal they will die. In fact the opposite happens when you fast but intermittent fasting done incorrectly is also damaging. 
  6. Persistent high-fat diets can change the gut microbiome. It has been shown that a high-fat diet can increase LPS producing bacteria in the bowel8
  7. LPS can increase the risk for insulin resistance and diabetes, overweight and obesity8.
  8. It is absurd to think that we as humans can eat anything in large quantities and not suffer any consequence. It is not about the quantity of fat consumed but the quality. It is important to consume adequate amounts of important Omega-3 fats and to decrease saturated and trans fats and Omega-6 fats from vegetable oils. 

Can Intermittent Fasting be used along

with a keto-like diet? 

 

Answer: A Definite YES!

  1. Intermittent fasting produces ketones the longer the fast lasts for 
  2. However, intermittent fasting can be done badly and there is a fine line between healthy fasting and malnutrition

 

Should the Keto Diet be personalised?

The answer is a resounding yes! Each individual will have their own unique genetic makeup, their unique microbiome and will have a unique metabolic profile. Any dietary approach needs to view you as an individual and not use a one-size-fits-all

This website is all about a personalised approach and precision nutrition. It is about using a keto-like approach but not suffering malnourishment or damage to your body . For such a personalised approach, we need data. Click on the Precision Nutrition link below to see how data specific to you is gathered for targeted dietary management. 

References

References

  1. Twigg, S. M., et al. (2007). "Prediabetes: a position statement from the Australian diabetes society and Australian diabetes educators association." Medical Journal of Australia 186(9): 461-465.
  2. Tabá, G., et al. (2012). "Prediabetes: A High-Risk State for Developing Diabetes." Lancet 379(9833): 2279-2290.
  3. The American Biology Teacher, Vol. 35, No. 3 (Mar., 1973), pp. 125-129
  4. Levine, M. E., et al. (2014). "Low protein intake is associated with a major reduction in IGF-1, cancer, and overall mortality in the 65 and younger but not older population." Cell Metabolism 19(3): 407-417.
  5. Salway, J. (2006). Medical biochemistry at a glance, Wiley-Blackwell.
  6. Velasquez, M., et al. (2016). "Trimethylamine N-oxide: the good, the bad and the unknown." Toxins 8(11): 326.Velasquez, M., et al. (2016). "Trimethylamine N-oxide: the good, the bad and the unknown." Toxins 8(11): 326.
  7. Erridge, C., et al. (2007). "A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation." The American journal of clinical nutrition 86(5): 1286-1292.
  8. Cani, P. D., et al. (2007). "Metabolic endotoxemia initiates obesity and insulin resistance." Diabetes 56(7): 1761-1772.