The Low-Carb Diet- What You Need to Know

Prof wrote a mini-series on the low-carb diet. Today, we have compiled her 8 entries into one article for reference.

1. Dear Facebook friends. As promised, I will start with the first writing of a mini series on the low carb, high fat diet. Also known as the ketogenic diets. A watershed publication appeared on the 16th of August in the very prestigious LANCET medical journal. The article, authored by Seidelmann and his collaborators addressed the topic 'Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analyses'. It is a highly powered longitudinal study that investigated 15000 free living subjects over 25 years. The study included 18 countries in 5 continents.The outcome was adjusted for age, sex, race, total energy consumption, diabetes, cigarette smoking, physical activity, income level and education. Both high (more than 70%) and low ( less than 40%) percentages of carbohydrate diets were observed to increase mortality, with the least risk observed at 50-55% carbohydrate intake. Life expectancy decreased most in the less than 30% carbohydrate group where protein was sourced from animals. In this group life expectancy decreased by a staggering 4 years throughout life. E.g. for a 46 year old, life expectancy was decreased to 42 years. Protein and fat derived from plant product in the low carbohydrate group resulted in a lesser effect, with life expectancy decreasing by 1.1 years. The high carbohydrate intake group (more than 70%) had a small but significant increase in all cause mortality.
In my next writing I will address the scientific flaws of the low carb diets. This will be followed by possible causes for the decrease in life expectancy. And finally how to take it from here.

2. Dear Facebook friends. In the second post of my mini series on the adverse impact of the low carb, high protein/ high fat diet, I need to first address the control of body fat mass. Unless there is a scientific understanding of how the body functions, the public will always be at the mercy of cult groups, sensationalists, people that make idle promises and those who profess to be so learned and filled with knowledge, that they can fly in the face of all that is scientific. Determination of body fat mass follows a brain centric model in the human. Not an isolated peripheral fat mass control model. So even though the function of fat storage and release of fat is to an extend executed by insulin, it is just another step in the much bigger and more complicated metabolism of determination of the body stat. This brings us to two crucial principles that must be understood. Firstly, the body stat cannot be manipulated by moving macronutrients around. Extremes of intake, or no intake, of e.g. carbs or protein cannot override the central control of appetite, satiety and energy expenditure. Various nuclei in the brain, together with the hypothalamus, will ultimately control your body stat. Secondly, insulin does not have some magical, isolated control of your fat mass. Statements such as 'it is your insulin resistance causing your overweight problem' or ' if we treat your insulin resistance your weight will improve' is incorrect and a display of how little is understood about your overweight. Likewise statements that macronutrient shift can force your body to use fat as a fuel, is incorrect and a display of ultimate lack of knowledge of how metabolism works. Like looking through a keyhole and professing that you have seen the whole room. In my next post, I will address how the sciences know that the above statements are incorrect and why taking in no, or little carbs, cannot lead to cellular starvation.

3. Dear facebook friends. In the third of my mini series on the low carbohydrate high fat high protein diet, I was going to pause a bit on how insulin works. I have however noted that I have received many messages of people arguing that a ketogenic diet is a less that 5 percent content of CHO intake and therefor not applicable to the 40 percent quoted in the Lancet study. This urges the following. Firstly, that there is still a poor understanding that arguing about 5 or 40 percent is futile. Fat mass is controlled principally by the brain's homeostatic powers and not by what happens at the level of the fat cel. Think of the process as an orchestra in which numerous instruments will be co-ordinated by the conductor, in this case very powerful signaling from the brain. Secondly, the Lancet article studied longevity and it indicated very powerfully that a less than 40 % CHO intake decreased survival. The main principal to understand is exactly that. Stop arguing about 5,10 or 40 percent. Swing your head around the fact that low CHO is not the way to go, and do this by looking at the big picture. Respected sciences will look at the following: basic science research and evidence, clinical outcomes and dangers and longterm documented outcome. Clear your mind and now lets start from a clean slate.

With the increased insulin secretion of obesity, type 2 diabetes and excessive refined sugar intake (not CHO intake per se), insulin will act by storing excess intake in various metabolically active cells. At the earliest, lowest level of increase of insulin on the logarithmic scale, it starts with fat tissue and as the level increases will move to muscle and liver. The next principal to understand is that this increase equates, at onset, normal physiology and that as long as you are still gaining weight you must be sensitive to some of the actions of this hormone. Elevated insulin levels does not equal insulin resistance! For practical purposes you can accept that insulin resistance has started at the first signs that your body is not handling glucose homeostasis any more.i.e. you have an elevated blood sugar that appears from time to time. Most patients will also give this history quiet accurately. 'Doctor I have been at this weight for 2 years now. I may go up or down by 10 kg but I cannot keep it down'. It is because your brain has now stored your previous highest weight molecularly down to a half kilo and will defend that weight by brain centric control of metabolism and various other homeostatic mechanisms.These pathways are magnificently elegant and complicated in its execution. At this point it can also be stated the concept of so called 'food addiction' is wrong and again a display of lack of insight into the brain's mechanisms of control. In my next delivery more about what happens during increased insulin secretion and what is important to know.

4. Dear FB friends. In the fourth post of our mini series in the low carb high fat/protein diet I am going to deal with some research speculations. First I want to refresh your memory about some physiological functions insulin has. It is the hormone that will store fuel such as glucose in the fat cel, but also be inhibiting breakdown. This pathway forms part of normal physiology to prevent us from running into trouble. These two pathways are called lipogenesis and lipolysis and insulin is therefor also known as the most important, but by no means the only! anti-lipolytic hormone. It has been speculated that during weight gain, as well as excessive sugar and refined carbohydrate intake (more than 70% of intake), insulin secretion increases and less of the breakdown product named free fatty acid (FFA) will appear in the blood stream. Some researchers have proposed that this lower level of FFA triggers a state of 'cellular starvation' that will cause a higher appetite and a slowing down of energy expenditure by for e.g. the liver and muscle. This will then conspire to driving obesity. Introducing a very low carb intake should then reduce insulin secretion, which in turn would lead to a supposedly higher rate of fat mobilization and more oxidation of FFA and then your speculative weight loss will follow. Herein lies flaw number one. Fantastic and very sophisticated whole body FFA turnover studies done by icons in the field of metabolism such as Prof Keith Frayn from the UK and Prof Peter Arner from the Karolinska Institute in Sweden, have shown that FFA levels in obesity is HIGH, not LOW. So despite our knowledge that higher insulin levels will lead to more lipogenesis, what is seen in obesity is an almost rampant FFA turnover. In a condition such as diabetes associated with obesity we have double trouble. Both a HIGH FFA and a HIGH glucose. Extending this pure scientific logic, a very high fat intake will have its own load of glycerol and FFA to add to the pool. With no proven 'cellular starvation' theory present in obesity metabolism, combined with a high influx of saturated fat, we now have a recipe for disaster. Read more about this and flaw number two in the follow-up posts.

5. Dear FB friends. It seems like the public is really struggling with the concept of insulin resistance. I therefore feel obliged to try and make this more clear and deal with all the misnomers. I also know that people do not read long text. So let me do them one at a time and in small bites...literally.

FACT 1. INSULIN RESISTANCE is never the cause but always the consequence of your weight problem. You cannot gain weight due to so called IR. It is a physical impossibility! The main action of insulin in the body is to form fat and then to keep it there. In order for this to happen your insulin must be working! Very hard..

6. Dear FB friends. In my fifth mini series on the low carb high fat diet I want to focus on the very serious consequence of cell death or also in the scientific world known as apoptosis. Under conditions of equilibrium, the metabolism in cells will be programmed to use the fatty acids we have produced or have taken in, to in turn produce ATP. This is the basic building block of energy. It is done through the beta-oxidation pathway. In the event of an excess of fatty acids, this pathway of oxidation is placed under stress and the body will react by opening up another, aberrant pathway, that will lead to rapid fat cell formation and proliferation, no matter where the fat tissue may form. It could be in the heart, liver, muscle or pancreas etc. Without delving into too many technic terminology of the interim steps, all you need to know is that an end product called ceramide will be formed. This is a very harmful molecule to the body and has the end result of cell death or apoptosis. This molecule has also been described in conditions such as cancer and can also be formed during inflammation. In the event that this molecule is produced in the pancreas, it will cause death of insulin producing cells and diabetes will start or worsen significantly. We must therefore understand that obese or diabetic patients attempting this diet could face the onset or worsening of diabetes, as it is extremely unlikely that they will follow a total calorie intake that is sufficiently low to prevent this pathway. In the next post we look at what else can happen in the pancreas.

7. Dear FB friends. On the ongoing topic of insulin resistance. I often have patients coming to me stating that they were told their 'bloods' showed that they have IR. So herewith misnomer number TWO. It is unfortunate that the commercial labs started using formulae such as the HOMA and Quicks index in the same context as IR. These formulas are mathematically invented models for use in a research setting, loosely signifying a diminished SENSITIVITY of insulin to glucose. It is easy to see how the misusing of these indexes with IR started, because at a first glance they look the same! But they are not! For clinical use these indexes are totally useless!! and have no relevance to 'what diet can be prescribed next' to 'fix it'...or far worse even, slapping the patient onto Metformin to 'correct their IR'. True IR can only be measured in a science laboratory with long and complicated clamp studies. Making use of the HbA1 as a clinical tool is far more useful, as a HbA1 of 5.7 to 6.4 indicates that you are pre diabetic. Outcome studies have shown a five fold progression to diabetes. So next time ask your doctor for your HbA1 level, forget about all the IR stories and forget about a diet that can 'fix your IR’.

8. Dear FB friends. This will be post number six and my final say on the low carb high fat high protein diet. I want to move onto other more interesting topics. The South African public had been grossly mislead by this diet and it is time to stop this ridiculous fad. A high saturated fat intake has been shown to not only cause apoptosis of many cells, including the beta cell of the pancreas, but can also decrease the clearance of insulin in the liver. This will lead to a drastic increase in insulin levels in the body to unacceptably high levels, as the liver is responsible for 40% of the clearance of insulin produced in the body. It will lead to overstimulation of the pancreas and eventually the beta cells will burn out and diabetes will ensue. But more importantly, it will stimulate the homeostatic and hedonic feeding pathways in the brain towards feeding. Have you ever wondered how people who was on this diet, start overeating on fruit, carbs and other sweet things as soon as they come of this ridiculous diet? Well now you have the answer. The brain has taken over and not in a good way. Fortunately there is bariatric surgery for people with a BMI over 30 and have become enlightened enough to understand that you are not going to fix this mess with yet another round of diets. Alternatively you can embrace the DASH diet and very serious cognitive behaviour modification therapy at a good centre. The success of the last option for people who have suffered from chronic obesity will be less than 5% over 5 y. The success of metabolic surgery- 50 times that. Why? Because 80% of how these ops work would be by fixing what has gone wrong through altering hormonal signals to brain, hind gut, pancreas, liver and muscle.

Featured Posts
Recent Posts
Search By Tags
Follow Us
  • Facebook Basic Square
  • Twitter Basic Square
  • Google+ Basic Square

© 2018 by CEMMS WC

  • Black Facebook Icon
  • Black Instagram Icon