Plateau …

To recap very briefly … Old couch potato is enticed onto a bicycle and it reawakens something within that has been dormant for quite a few years and he likes it.

The regime goes something like this …

  • cycle 5 days a week – average 250 km/week in recent weeks.
  • weight training 2 days a week.
  • Diet – low carb high fat (keto) ovo-lacto-vegetarian, lunch and evening meal nuts in between (usually no breakfast). Protein supplementation to reach ~1.5g/kg of ideal weight.

No calories have been counted.

Too many progress reports would become boring but not enough could give the impression that I was trying to conceal a failure.

Initially, as always, the weight simply fell off …I weighed myself the day I bought the first bike. The diet started three weeks later. The dots represent every Monday since. Somehow I always seem to weigh more on Mondays than on other days, how does that work? If I changed days would that phenomenon follow me?

About five weeks ago the weight loss ground to a halt. 13 kg of ugly weight gone – a guillotine could not have done better (average weight of a human head is only 5kg). Along with it went more than four inches from my waist.

A successful diet is one where an overweight person intentionally loses more than 10% of their body weight – 11kg of 93 = 12% – and keeps it off for more than a year. The foundational study by Stunkard and McLaren-Hume 1959 found that of 100 obese individuals only 2 were in fact successful.

So this is the time to ponder a few important questions.

  • Why does weight loss stop?
  • What can be done to prevent a big bouncing relapse?

It takes a certain amount of food to maintain a particular weight in the presence of a certain amount of exercise. That’s simple enough but how much varies from person to person and even for one person at different weights. So consider firstly the unlikely case of someone eating the same number of Calories and doing exactly the same amount of work every day. Let’s assume that at the outset Calories in is less than Calories out – the stage is set for weight loss.

There are two forms of energy store in the body glycogen and fat. Glycogen is stored in the liver and muscles.  It is readily available energy, the first to go on a diet and it takes three times its weight of water with it. That’s the easy part. Once we get onto mobilising fat things slow down.

But progress goes on. As weight is lost the energy cost of the work done decreases and the size of the Calorie deficit decreases with it. Weight loss slows and will eventually stop.

In reality it stops well before the point that simple maths predicts for a number of reasons. Humans have not always existed in a world awash with food. We have evolved mechanisms that help us survive food shortages, endure periods of starvation. The recently emptied fat cells pump out lipoprotein lipase, which tells  the brain “hey, we’re starving”. Leptin, the hormone that tells us we have eaten a sufficiency, diminishes. Ghrelin, the hormone that makes your tummy grumble, increases. Peptide tyrosine-tyrosine and cholecystokinine increase. These things conspire to increase your appetite.

Meanwhile the resting metabolic rate goes down in response to reduced thyroid hormone (T3)  and reduced activity in the sympathetic nervous system. Levels of a group of proteins that uncouple metabolism from energy production (analogous to wasting petrol by revving the engine with the clutch disengaged) diminish. In the good times some excess energy was simply turned into heat now faced with a famine nothing is being wasted.

Yet more energy can be saved by reducing nonessential activity.

When the recently obese person is compared to a never obese person of the same weight and body composition their energy economy is quite different. All the differences are to the dieters’ disadvantage. Failure beckons and I’ve traveled that route before.

However, only 98% fail.

So far I’ve relied rather heavily on Exercise Physiology for Health, Fitness and Performance by Sharon Plowman and Denise Smith. The next section owes much to a paper by Wing and Phelan which can be found <HERE>.

They paint a picture that is less bleak, as many as 20% manage to keep the weight off, and they present some of the characteristics of those that do identifying six key strategies for long-term success at weight loss …

  1. engaging in high levels of physical activity;
  2. eating a diet that is low in calories and fat;
  3. eating breakfast;
  4.  self-monitoring weight on a regular basis;
  5. maintaining a consistent eating pattern; and
  6. catching “slips” before they turn into larger regains.

In addition those who initiated weight loss because of a medical trigger such as a relative having a heart attack were more likely to succeed.

Holidays and weekends are dangerous moments and those that maintain the same regime through these periods as they do the rest of the time do best. Once relapse is underway prospects are poor. Depression bodes ill.

I can put a tick against items 1, 4 and 5. Item 6 is really what item 4 is all about and hasn’t yet been put to the test. My most obvious vulnerability is relying on satiety to determine portion size.

But, oh dear, a low fat diet and eating breakfast are not on the agenda.

I have no doubt that these are common practices in those that succeed in long term weight maintenance but my conjecture is that these have not contributed to their success. Clearly these are remarkably self disciplined people. The discipline they have imposed on themselves is a very orthodox one. Dr John Harvey Kellogg told the world that breakfast is the most important meal of the day to the certain benefit of the food producers but there is no evidence that it is to the benefit of the rest of us. On the other hand there is some evidence in favour of intermittent fasting. I tend not to eat after 9pm and defer breakfast until noon giving my pancreas a 15 hour rest on the majority of days.

Fear of fat is another well entrenched orthodoxy. I’ve lost weight on a high fat diet. It defies logic that I can’t maintain weight on a high fat diet.

These two points are examples of well-person confounders – baggage that is carried along with useful characteristics that really do contribute to health.

Or at least I hope that’s the case!

Keep Living Fast …

If you are overweight or obese your chances of dying of any cause are raised.

From – Body-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continents. Lancet. Aug 2016.

If you were one of the nearly four million people in this study the best weight to be was the one that put your Body/Mass Index under the red arrow. As it goes up or down so too do your chances of dying. It’s a J curve.

If you are young and obese you have the most to gain from losing weight. It is not easy but some succeed. You can give it a go or you can shriek about fat shaming and stuff another ice cream in your face.

If you’re obese and really lucky you may be metabolically healthy. It’s true for a minority. On the other hand some people of normal weight fall prey to those ills we associate with obesity, the dreaded metabolic syndrome. It does rather complicate the decision regarding the ice cream.

But wait it gets worse.

If you are a baby boomer or, my goodness, even older there are a number of confounding issues. Declining muscle mass being replaced with fat can bring all the disadvantages of obesity at a normal or not greatly elevated BMI. Add to that the fat distribution – middle aged spread tends to go around the middle where it does more harm than subcutaneous fat. You may be in more trouble than you think … or less.

I’m still exactly the same height I was lying about when I was 18 but some people have shrunk. This would increase their apparent BMI even if they haven’t put on a gram in the meanwhile. (Do I get extra consideration for bow legs?).

Next thing to consider is the obesity paradox. If BMI is plotted against all cause mortality in the elderly a different picture emerges than the one above. A higher BMI can appear to be protective. The simplest explanation for this is that death is fairly common in this age group and is often preceded by a period of wasting. Alternatively it may be because those most susceptible to the ills of obesity have already been eliminated from the cohort.

So if unintentional weight loss clouds the picture is intentional weight loss safe or not?

Intentional weight loss, even when excess fat mass is targeted also includes accelerated muscle loss which has been shown in older persons to correlate negatively with functional capacity for independent living. Sarcopenic obesity, the coexistence of diminished lean mass and increased fat mass, characterizes a population particularly at risk for functional impairment …. Miller & Wolfe.

Failed weight loss in a sedentary population invites the worst of both worlds – lose fat and muscle regain only fat. Weight loss in the elderly regardless of intentionality also  carries an increased risk of subsequent hip fracture.

No surprise then that health care professionals are divided on whether weight loss should be recommended to their elderly patients.

This little essay draws heavily on a review paper by Gill, Bartels & Batsis.  Their conclusion is fairly positive …

The number of older adults is projected to increase substantially in the coming decades and addressing obesity is essential for the health of this rapidly growing population. Though the “obesity paradox” has contributed to a lack of attention to addressing obesity as a major health problem in older adults, weight loss and improved fitness in obese older adults has been shown to improve function and multiple health indicators. Though physical activity and diet alone can improve outcomes, randomized controlled trials showed better outcomes when they were combined. The process of activity prescription should be patient-centered in order to develop a plan that is relevant to the older adult’s goals and achieve the overarching purpose of improved quality of life.

If you’re no spring chicken and thinking of shedding some weight it’s worth a read. A chat with your doctor would also be a good idea. Diet and exercise beats either alone.

My choice was to start cycling coupled with resistance training and a low-carb diet taking care to keep the protein intake up. All appears to be going well, the hips are still intact (you’d need oxy-acetylene equipment to get through one of them).

Previous failure has taught me that it ain’t over until the fat lady is singing about how much weight she’s lost but cycling is low impact compared to running and the keto diet involves little will power compared to calorie restriction diets. Confidence remains high.

Live Fast …

… Die young. I have no particular objection to the first half of that particular motto but even as a youngster didn’t feel a great affinity with the second half. Nor has it been popular generally – not dying young is the reason we have a population that is on average getting older.

But, as I’ve said before, if I can have some extra please insert it in the middle not add it on the end. Anywhere in the healthspan will do fine just not on the lingering tail of the lifespan.

Increased life expectancy has largely been the result of public health measures, road safety legislation, improved medical services and an avoidance of widespread warfare. It’s all about keeping us from dying. Enjoying good health is quite distinct from merely surviving. This is where the user pays principle in healthcare cannot be avoided. It’s your body.  You will pay for what you do with it.

As a community we have shown a willingness to look after ourselves. Our intentions are good. We have, in the main, listened to good advice and reduced our smoking. We have also listened to dietary advice. Consumption of those things that we have been urged to reduce has gone down but nonetheless our weight has gone up. I think US data is good for Australia as well.

And the timing of the obesity pandemic is a bit suspicious …

If I were defending the guidelines I’d be quick to point out that correlation is not proof of causation but hey, saturated fat was convicted on flimsier evidence than this.

So was it bad advice or simply an unequal battle against sugar – cheap, addictive and toxic? Nowhere in the guidelines did it say eat more calories but that is indeed what we’re doing.

Or is it, instead, a function of our ageing, a collective middle aged spread? If we turn our heads one morning, catch sight of our belly in profile and achieve enlightenment what should we do about it?

Where Dreams Go To Die …

As mountaineers ascend the world’s highest peaks they know that above 8,000 metres they have entered the death zone. At this level oxygen is so scarce that the human body can no longer acclimatise. Indeed the highest permanent human habitation is a fair bit lower – La Rinconada in the Peruvian Andes at 5,100 meters.

Time in the death zone is at a premium, the climber must achieve their goal and descend. To remain long is to die.

So it is with my weight loss diets. Somewhere between 5,000 and 8,000 grams my body ceases to acclimatise. Progress ceases and the journey downhill begins. The summit beckons, I linger hoping that I will find the strength to continue but alas it was never to be.

In this I am not alone …

A search was conducted for weight-loss-focused randomized clinical trials with >or=1-year follow-up. Eighty studies were identified and are included in the evidence table.

… A mean weight loss of 5 to 8.5 kg (5% to 9%) was observed during the first 6 months from interventions involving a reduced-energy diet and/or weight-loss medications with weight plateaus at approximately 6 months. In studies extending to 48 months, a mean 3 to 6 kg (3% to 6%) of weight loss was maintained with none of the groups experiencing weight regain to baseline. In contrast, advice-only and exercise-alone groups experienced minimal weight loss at any time point.  Franz et al.

I started cycling five months ago. The distance covered each week has slowly increased. Last week it passed 200 km for the first time. The one long ride each week has also increased. The longest so far is 80 km. A kilogram a month melted without conscious dietary modification over the first three months. I have now been on a low carb high fat diet for two months and a further six kilograms have departed.

Is my diet in the death zone?

It doesn’t feel like it. My trousers are walking around looking for a decent bum to fill them, my belt is distraught at the loss of the companion that for so long bore its imprint  but I feel good. Per ardua ad astra. Carpe diem. Et cetera.

The greatest challenge is ahead.

Glycogen Dethroned …?

A couple of weeks ago I wrote Running on Fat in which I said that glycogen was king. The current paradigm can be summed up as things go better with carbs. That is before during and after. Muscle glycogen depletion during  exercise is the main factor in the onset of fatigue.  If you want to exercise again in a hurry you need to get some carbs down in a hurry. The amount and type vary from paper to paper and there is an unresolved debate about the addition of protein. Overall though it is suggested that 6 to 12 grams of carbohydrate per kilogram within 30 minutes of completing an exhausting workout should have you ready to go again the next day.

Since my muscles are not being rewarded for their efforts with a jar of marmalade after every session I have been wondering how much of a disadvantage I’m putting them at. And it’s not that easy to find out.

Some short term research has been done putting normal (high carb) athletes on low carb diets for three weeks and watching their performance suffer. Hardly surprising that it goes down hill it takes a few weeks to sort out your fluid and electrolyte balance and adjust to ketosis.

The body can make it’s own glucose from fat and if it’s starving it can turn to protein. In the absence of ingested carbohydrate does glycogen replacement grind to a halt or does gluconeogenesis step into the breach?

I was pleased to come across a paper by Volek et al describing research with 20 well matched elite athletes 10 of whom were regular high carb guys and 10 were low carbers (and had been for at least 9 months). Naturally, when you get your hands on such a group, you take muscle biopsies and put them on a treadmill for three hours, take more muscle biopsies and measure everything you can think of. Then you give them two hours to recover before taking another muscle biopsy!

The rate of fat oxidation was two to three times higher in the low carb athletes and it peaked at a higher level of effort. Glycogen stores, usage and replacement were very much the same in both groups.

Their conclusion …

Compared to highly trained ultra-endurance athletes consuming an HC (High Carb) diet, long-term keto-adaptation results in extraordinarily high rates of fat oxidation, whereas muscle glycogen utilization and repletion patterns during and after a 3 hour run are similar.

At the ultra marathon level the benefits of using fat as fuel are appealing to more and more competitors, you just don’t run out.

Metabolic Goodness …

It was my long ride this morning. In fact my longest in this incarnation of my cycling career. 80 km. Thirty years ago I would have made sure I ate a good breakfast and would have taken a banana or two and some other snacks perhaps. This morning was devoid of breakfast and there were no snacks en route. I just took plenty of fat, all stored internally and it will be a long time before that runs out!

After my low carb lunch my ketones were ~6mm/litre. My fat cells are throwing ketones around like the missus spends my money, my muscle cells by comparison are as tight as Mr Scrooge. (Forgive me Gayle I know you are very sensible with our money and I’m the one that throws it around).

The reason that fat cells waste energy when ketones are present whilst muscle cells, including heart muscle, are very efficient are complex. Dr Bikman explains this as clearly as is humanly possible …

He has a book coming out in a few months entitled Why We Get Sick. Spoiler – it’s because of insulin resistance but it will be very interesting to read what he has to say about that and I expect it will be remarkably lucid.

Ketosis …

In my recent reading I came across a paper in the medical literature than mentioned ketosis and followed that in brackets with ketoacidosis as though the two were synonymous. How dumb is that I thought and moved on. Now I can’t find it again and dumb is not a useful search term – way too many results.

On a carb restricted diet the body produces a group of chemicals called ketones, hence the keto in keto diet. Ketones are excellent fuel for the brain and heart in the absence of normal amounts of glucose. Our ancestors went through lean times it was ketones that got them through. Nutritional ketosis is a normal response to fasting and carbohydrate restriction.

Ketoacidosis on the other hand is a medical emergency. It occurs mostly in people with type 1 diabetes mellitus. Ketones are present at more than ten times the quantity found in dietary ketosis along with very high blood sugar. The combination causes a pH change in the blood which will bring liver and kidney function into a downward spiral. This is sometimes the way that diabetics first present and remains a risk if patients fail to manage their insulin properly or hit the booze. Death is the likely outcome in the absence of prompt treatment.

Type 1 diabetes occurs because the islet cells in the pancreas that make insulin are snuffed out by the body’s own antibodies. If there are still some functional islet cells ketoacidosis is less likely.

What stops the enthusiastic keto dieter from slipping into ketoacidosis? Two things. On a low carb diet blood sugar is not through the roof. Secondly functional islet cells mean that insulin is available when needed. Insulin doesn’t only regulate glucose it can also turn down the production of ketones. Ketosis is a normal functional response so it is hardly surprising that it is well regulated.

My low carb diet is rolling along quite nicely. A reduction of five inches off my circumference is evidence enough that I am maintaining an effective level of ketosis but it is easy to check. Ketones can be measured in blood, breath or urine. There is a good article on the available technologies at Diet Doctor. Given that I have no interest in checking every day for the rest of my life I opted for the low tech urine sticks. The brand available at the local pharmacy is Keto-Diastix which measures glucose and ketones and gives a numerical result. I am pleased to say that glucose has been absent from my urine, as it should be, whilst ketones have ranged from 1.5 to 4.0 mm/litre.

I have departed the ranks of the obese and I am now proudly overweight!

Salt …

It’s been traded, taxed, fought over. It’s been ploughed into the fields of defeated city states. It is used in some religious ceremonies. It is essential to life and one of the fundamental tastes mediated by the human tongue. It’s the difference between a herring and a kipper, pork and bacon because it is an effective preservative.  It has been used as currency and it gives us the word salary (although the Roman Army was never paid in salt).

Solntsata in Bulgaria was possibly the first city in Europe. The name translates as salt works and they have been in use since 5400 BC. There is evidence of even older salt extraction processes in China.

Cheetham Saltworks, Victoria

It is essential to our physiology, without it we couldn’t even generate a nerve impulse. But In excess it increases blood pressure which in turn increases the risk of heart disease and stroke. So how much is the right much?

The Australian guidelines are formulated by the National Health and Medical Research Council and can be accessed at this government website which also sets out the logic behind the recommendations. They deal in milligrams of sodium. Salt is sodium chloride. 1 unit of sodium = approximately 2.5 units of salt once you add the chloride.

The suggested daily target is 2 grams of sodium a day for adults (roughly 5 grams of salt). The NH&MRC wrestled with an upper limit but concluded that

…  because the relationship between sodium intake and blood pressure is progressive and continuous, it is difficult to set a UL precisely.

So no upper limit was set.

The average Australian is ingesting about 9 grams of salt a day currently. Some is an inescapable part of the raw ingredients of our diet but much of that figure is added to restaurant and take away food, processed and packaged food, and drinks such as Coca Cola and sports drinks. It makes food more palatable by dialing down the sensations of bitterness and over sweetness. In the case of drinks it increases thirst – how convenient for the manufacturers.

So far as it goes the NH&MRC guideline purports to have an evidence base, is easy to understand and is aimed at getting the community’s blood pressure down.

The low carb intelligentsia seem to give the issue very little concern. How come?

A low carb diet has a real food base. McDonalds is out. Most packaged foods are out. If you start with the raw ingredients of a keto diet the challenge is to get enough salt especially if you are also into sweaty exercise.

The phrase lower limit doesn’t occur in the government website. Whilst the essential nature of salt is acknowledged the assumption seems to be that less is best. There is evidence to the contrary.

An article by Mente and an insane number of other authors (28 other authors – I imagine they wrote every 29th word and then had a committee meeting on where to put the punctuation marks) )from the Lancet May 2016 entitled Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: A pooled analysis of data from four studies, reports on a study of 133,118 individuals roughly half of whom were hypertensive. The daily intake of salt was compared to the likelihood of death and major cardiovascular events and blood pressure over a median period of 4.2 years.

Compared with moderate sodium intake, high sodium intake is associated with an increased risk of cardiovascular events and death in hypertensive populations (no association in normotensive population), while the association of low sodium intake with increased risk of cardiovascular events and death is observed in those with or without hypertension.

There is a subtlety there that I will return to but first let’s take a look at the results as a graph …

On the vertical axis we have the hazard ratio, on the horizontal axis the daily excretion of sodium in mg. Daily excretion of sodium is pretty much the same thing as daily intake of sodium. The amount of  sodium in blood is regulated by the kidneys and there is no storage mechanism. The U-shaped curve comes as no surprise, sodium is essential therefore as you reduce the intake you’d expect to reach a point where risk starts to increase. Excretion of less than 3g of sodium a day increases the risk of cardiovascular catastrophes and death. The graph shows that the risk increases above 7g a day. The lowest point of the curve falls between 4000 mg and 6000mg of sodium or ~11 grams of salt.

If instead of looking at the whole cohort we look at the hypertensive and normotensive subgroups steepness to the left of the low point stays the same for both but to the right it rises more steeply for those with high blood pressure. Why should this be?

The kidneys play a pivotal role in the maintenance of blood pressure and not all kidneys are equal. Researchers have bred salt sensitive rats that develop high blood pressure. If their kidneys are transplanted into normal rats the recipients develop high blood pressure on a high sodium diet. Normal rats receiving kidneys from normal rats do far better. The problem follows the kidney. This is borne out in human transplantation as well. If the donor has a family history of hypertension the recipient has a ten fold increased risk of developing hypertension.

Mente et al looks like a pretty robust study. If we accept their findings it follows that –

  • The Australian public are not far from an ideal salt intake.
  • The NH&MRC guidelines are set at a level which will increase risk.
  • and unless you have hypertension there are more important things to think about.

If only things were that easy. Not all studies bear this out. Cook et al

found an increased risk at high sodium intake and a direct relation with total mortality even at the lowest levels of sodium intake.

They suggest that other studies are in error …

While several studies suggest beneficial effects of lower sodium on cardiovascular disease, the relationship with total mortality remains controversial. Some have reported a J-shaped curve, but this may be due to poor quality measurement of sodium or confounding bias.

Clearly the definitive answer still eludes us although I am suspicious of any study of an essential nutrient that doesn’t find detriment at a low level of intake.

Which study do we choose to ignore?

I think the best strategy is to ignore neither despite their contradiction. Rather we should take our blood pressure. It’s easily done at home. The hypothetical guy I studied in Physiology weighed 74kg had a pulse rate of 72 and a BP of 120/80. Blood pressure tends to rise through life and the doctor tends to reach for his prescription pad at about 140/90. If you’re border line and want to stave off the pills there are some non-drug remedies to consider …

  • Lose weight
  • Exercise
  • Reduce your salt intake

If you’ve got it to lose then 10 kg off should drop your BP by about 10 mm of mercury. For each gram reduction of salt a hypertensive person can hope to drop about 2 mm of mercury.

William Banting …

Good old King George lll died at Windsor Castle at 8.38 pm on the 29th of January, 1820. He’d  been completely out of his mind for about a decade. He was buried in St Georges Chapel in the castle on the 16th of February. The undertaker was 5 feet 5 inches tall and about 5 feet 5 inches round.

These are the sort of details you have come to expect of McGee, though I confess that I made up the last one although it might have been close to the mark.

The undertaker in question was William Banting (1796 – 1878). He was much troubled by his weight, in 1863 he wrote …

Few men have led a more active life—bodily or mentally—from a constitutional anxiety for regularity, precision, and order, during fifty years business career, from which I have now retired, so that my corpulence and subsequent obesity was not through neglect of necessary bodily activity, nor from excessive eating, drinking, or self-indulgence of any kind, except that I partook of the simple aliments of bread, milk, butter, beer, sugar, and potatoes more freely than my aged nature required …

He had tried diet and exercise and a number of treatments we would find odd today such as taking the waters at various spas. At one stage of his life he was rowing a boat on the Thames every day before work but it made him so hungry it was doing more harm than good. Eminent doctors were consulted but to no avail.

Obesity seems to me very little understood or properly appreciated by the faculty and the public generally, or the former would long ere this have hit upon the cause for so lamentable a disease, and applied effective remedies, whilst the latter would have spared their injudicious indulgence in remarks and sneers, frequently painful in society, and which, even on the strongest mind, have an unhappy tendency …

Not a lot’s changed really.

Enter Dr William Harvey of Soho Square who prescribed a diet …

The items from which I was advised to abstain as much as possible were : —Bread, butter, milk, sugar, beer, and potatoes

By the time William was ready for bed he’d eaten about a pound (0.5 kg) of various dead animals, one serve of vegetables other than potato and a couple of ounces of dry toast. He’d drunk unlimited quantities of tea with no milk or sugar, half a dozen glasses of claret and a brandy, the first known keto diet published in the English language.

He tells us that he was 5 feet 5 inches tall and weighed 202 pounds (BMI 33.6). The weight and the girth dropped off. The undertaker to royalty was delighted …

I have not felt so well as now for the last twenty years.

Have suffered no inconvenience whatever in the probational remedy.

Am reduced many inches in bulk, and 35 lbs. in weight in thirty-eight weeks.

Come down stairs forward naturally, with perfect ease.

Go up stairs and take ordinary exercise freely, without the slightest inconvenience.

Can perform every necessary office for myself.

He tossed an extra fifty quid in the direction of Dr Harvey to use for the benefit of various hospitals and wrote and published a pamphlet, distributed free of charge so that others might share the benefits.

The Letter on Corpulence, Addressed to the Public ran into several editions and can still be downloaded. Subsequent editions were updated with further weight loss, reaching 46 pounds from a starting point of 202. He lost a little over 12 inches from his waist. (BMI 26).

I put on my former clothing, over what I now wear, which was a thoroughly convincing proof of the remarkable change. These important desiderata have been attained by the most easy and comfortable means, with but little medicine, and almost entirely by a system of diet that formerly I should have thought dangerously generous.


The Low Carb Pioneers …

Pass me some whale please, darling.

The traditional Inuit diet consists of marine mammal plus or minus fish. No bread, no potatoes not even some Brussels Sprouts. Liver, of course, has some glycogen but all the same it’s a very low carb high fat diet. For just a couple of months a year they could add some berries, grasses, tubers, roots, stems and seaweed. It was for a lifetime and it kept them very well. Heart disease and diabetes were uncommon.

Arctic explorer Vilhjalmur Stefansson was impressed with the diet and subsequently wrote …

In 1906 I went to the Arctic with the food tastes and beliefs of the average American. By 1918, after eleven years living as an Eskimo among Eskimos, I had learned things which caused me to shed most of those beliefs …

At the beginning of our northern work in 1906 it was the accepted view among doctors and dietitians that man cannot live on meat alone. They believed specifically that a group of serious diseases were either caused directly by meat or preventable only by vegetables.  Stefansson.

His views on the diet were largely dismissed, even the notion that he had actually survived on it.  The prevailing view was “… you are likelier to meet a thousand liars than one miracle.”

He proved his point when he and a colleague took up supervised residence at New York’s Bellevue hospital and resumed the diet. Subsequent medical examination pronounced him healthy.

There is another experiment going on. The standard American diet has found its way into the modern Inuit communities. There are now few eating a traditional Inuit diet but Sheehy and others have compared some that remain more traditional with others that are getting more carbs. They conclude that

Consumption of traditional foods is associated with greater diet quality and dietary adequacy.

Heart disease, diabetes and dental caries are on the rise for the Inuit.

We have so thoroughly learned that fat is bad that othodoxy still can’t believe “the miracle”.

And yet despite the fact that the high-fat Arctic diet may sound like a heart attack waiting to happen, the Inuit tend to have low rates of heart disease and diabetes.

That’s from The Salt discussing the role genetics may play in this amazing feat. It would be surprising if genetics had no role in adapting the Inuit to their environment but more importantly that little quote reveals the bias of the orthodox mindset. Instead of seeing this as yet more evidence of the benefits of a low carb high fat diet they are looking for the catch. They are warning us off the keto diet rather than warning the Inuit off the SAD diet.

Who are you gonna believe the dietary guidelines or your lying eyes?