The idea that "salt is bad for you" is entrenched in the American mindset; sodium's right up there with trans fats and cigarettes. We now commonly see ads warning us of the high sodium content of processed foods.

 I take the idea …"that a normally healthy person should restrict salt"… with a grain of salt.
i.e. to take a statement with 'a grain of salt' or 'a pinch of salt' means to maintain a degree of skepticism about its truth. The phrase has been in use in English since the 17th century;

In reality, the IDEA THAT SALT IS BAD FOR US IS NOT (and has never been) BASED ON SOLID EVIDENCE. Even worse, the idea is dangerously wrong: we need salt to live, and not eating enough can make a person die.

Salt does not cause our bodies to gain or lose fat.
Salt has no calories.

High consumption of salt only results in temporary weight gain as it causes the body to retain water. Low consumption of salt can result in temporary weight loss as it causes the body to expel water. It is normal and healthy to see these water weight fluctuations.

Our blood is 0.9% salt and it is continually flowing through our lymphatic system. Salt is also necessary for the production of hydrochloric acid, the digestive enzyme secreted by the stomach in order to digest protein. It’s important for nerves and muscles. When we sweat we can taste the salt coming out of our skin. Salt is vital for life’s existence. Put a salt block outside and all animals will consume it.

A diet low in salt can eventually lead to dehydration. Salt holds water in the body, and without it, people can actually dehydrate and die even while drinking water.

The anti-salt campaign began in the 70s, based on two pieces of flimsy research. Although researchers quietly acknowledged that the data were 'inconclusive and contradictory' or 'inconsistent and contradictory'... publicly, the link between salt and blood pressure was upgraded from hypothesis to fact, probably because there was no other good suspect at the time to blame for hypertension.

After studying new research conducted since 2005, a committee commissioned by the Institute of Medicine and CDC issued a report that "said there was no rationale for anyone to aim for sodium levels below 2,300 milligrams a day" .

One study found that among people with moderate to severe heart failure, those who consumed less salt were more than three times more likely to be readmitted to the hospital; another found that older folks with high blood pressure consuming less than 3,000 mg of sodium a day were as likely to suffer heart problems and strokes as those eating more than 7,000 mg a day. The average, across cultures and generations, is around 3,700 mg, suggesting this is probably around a naturally healthy range.

Despite this evidence, the American Heart Association has not amended its low-sodium recommendations.

Here’s an recent article by a medical professional about this subject.

To Salt or Not To Salt
        by Dr. Ayra Sharma, M.D. - May 20, 2013

Unbeknownst to many readers, the first 10 years of my research career was built largely on studying the effects of salt (or rather sodium chloride) on blood pressure.

In over 40 peer-reviewed publications, we described in excruciating detail the physiological effects of increasing and decreasing sodium intake, in many cases using single-blind randomised trial designs in hundreds of volunteers.

We not only examined the effects of salt on blood pressure but also on a wide range of physiological, metabolic and psychological parameters. We studied the effects on acid-base balance, we conducted genetic studies, we even performed in vitro studies on cells cultured from “salt-sensitive” and “salt-resistant” individuals.

In many respects, these studies left me as confused about the role of sodium on these parameters as I was before. Not that we did not report findings that helped us better understand the complex physiology of sodium homeostasis – it is just that we failed to convincingly demonstrate any major health implications of these findings.

In some cases we even reported adverse consequences of sodium restriction resulting both in significant elevations in plasma lipids and insulin resistance (perhaps not surprising given that reducing sodium intake markedly stimulates both the sympathetic and renin-angiotensin systems – the very systems we seek to block to reduce cardiovascular risk).

That was almost 20 years ago – the field does not appear to be much clearer today.

Thus, although surprising to some, I must admit that I was by no means surprised by the report on sodium released last week by the Institute of Medicine, with the rather revealing conclusion that,

“…the evidence from studies on direct health outcomes was insufficient and inconsistent regarding an association between sodium intake below 2,300 mg per day and benefit or risk of CVD outcomes (including stroke and CVD mortality) or all-cause mortality in the general U.S. population.” (or any other population for that matter)

This is not to deny that despite considerable methodological problems (not least in the actual measurement of salt intake), there is evidence to support the idea that higher salt intake may affect blood pressure and possibly cardiovascular risk. However, the data is certainly far less conclusive than food bloggers and health activists would lead us to be believe.

Not surprisingly, the same activists and organizations are now up in arms stopping just short of criticizing the scientific credibility of the IOM expert committee – no doubt, the same folks would have been applauding the conclusions of this “illustrious panel”, had the findings been more in line with their own activist agendas.

What is perhaps even more infuriating to those who have always considered the issue of sodium recommendations a slam-dunk case is the statement by the IOM that, there is in fact no basis on which to draw recommendations for the general public in recognition of the fact that significant proportions of the population may require higher sodium intakes and may even be likely to suffer harm from overly enthusiastic sodium restriction.

While I have no illusions that this report will in any way put the century old debate to rest (indeed the report calls for further research), I think that there is a much bigger message in this report that should let us tread cautiously when it comes to dietary recommendations in general.

Let us remember that associations (on which so many of our assumptions about healthy diets depend) simply do not prove causality, even when backed by seemingly plausible biological hypotheses derived largely from rodent toxicology.

We should also remember that fancy statistical predictions on the vast number of lives lost or saved by altering the population intake of this or the other nutrient, are generally based on sometimes rather heroic assumptions that may well explain whey they are rarely (if ever) borne out by actual interventions.

Thus, whether we are talking about salt, fat, carbs, sugar, fiber, gluten, calcium, Vit D, dairy or red-meat, a degree of humility in advocating for policies and other measures to reduce or increase this or the other is generally in order.

Seldom in the field of nutrition are things as cut and dried as some will have us believe – if only food were as simple as tobacco.

                          Dr. Sharma’s Obesity Notes – www. drsharma.ca
 

 

Here is a recent Quote by a member of a forum that I frequent.

(The article posted below) “supports what some say, and I contend,
about dieting for MOST--not all --. And by dieting I mean a purposeful restriction of foods and amounts to match a target low intake and weight goal.

It certainly doesn't mean that reducing the number of calories won't result in some weight loss. It will. The point is that as a strategy it has not been shown to change permanent habits in most who try it. Worse, it distorts the process so that weight gain statistically follows.

You can argue until you're blue in the face that it will work, but if it thwarts the natural process for most, I call that a strategy meant for the few. And the stats show it. Not for those who make it- for those who don't. Which is most.”

My response to this quote, and to the Article I've posted below is:

Everything that has to do with eating or not eating food is a Diet.

Eating LESS than the body uses as energy is a “weight-loss diet”
Eating the SAME food that the body uses as energy is a “maintenance” diet.
Eating MORE food than the body uses as energy is a “weight-gain” diet.

Some Diets are more easily incorporated into the lifestyles of Some People than other Diets.
Labeling any type of eating (but especially a plan to eat less) "not a diet"
or a “non diet” is just a Semantic Game.

No matter what the "Diet"... "eating plan" .... "way-of-eating" .... "lifestyle",
it is difficult to lose weight, and even more difficult to maintain weight-loss.

I've been saying this here at DietHobby and other online places for quite some time,
and the article below supports this.  

This is my personal experience, and
I've been researching and writing about this for quite some time.
Some of the writings that support this principle can be found at the Links below:

Rethinking Thin: The New Science of Weight Loss---and the Myths and Realities of Dieting (2008) by Gina Kolata.

No Cure

Effort Shock

Science Has Failed

The Fat Trap

The Fat Trap - Follow-up

The Chubby Side of Normal

Set Point

Do Diets Work?

The only "conventional wisdom" that's really "changed"
in the 6 years since the writing of this 2007 article posted below,
is that recent studies have indicated that exercise does very little to help one lose weight;
that exercise might be helpful in maintaining weight-loss;
however, that exercise leads to better physical and mental health.

Dieting Does Not Work, UCLA Researchers Report
                    by Stuart Wolpert - April 03, 2007 - UCLA News

Will you lose weight and keep it off if you diet? No, probably not, UCLA researchers report in the April issue of American Psychologist, the journal of the American Psychological Association.

"You can initially lose 5 to 10 percent of your weight on any number of diets, but then the weight comes back," said Traci Mann, UCLA associate professor of psychology and lead author of the study. "We found that the majority of people regained all the weight, plus more. Sustained weight loss was found only in a small minority of participants, while complete weight regain was found in the majority. Diets do not lead to sustained weight loss or health benefits for the majority of people."

Mann and her co-authors conducted the most comprehensive and rigorous analysis of diet studies, analyzing 31 long-term studies.

"What happens to people on diets in the long run?" Mann asked. "Would they have been better off to not go on a diet at all? We decided to dig up and analyze every study that followed people on diets for two to five years. We concluded most of them would have been better off not going on the diet at all. Their weight would be pretty much the same, and their bodies would not suffer the wear and tear from losing weight and gaining it all back."

People on diets typically lose 5 to 10 percent of their starting weight in the first six months, the researchers found. However, at least one-third to two-thirds of people on diets regain more weight than they lost within four or five years, and the true number may well be significantly higher, they said.

"Although the findings reported give a bleak picture of the effectiveness of diets, there are reasons why the actual effectiveness of diets is even worse," Mann said.

Mann said that certain factors biased the diet studies to make them appear more effective than they really were. For one, many participants self-reported their weight by phone or mail rather than having their weight measured on a scale by an impartial source. Also, the studies have very low follow-up rates — eight of the studies had follow-up rates lower than 50 percent, and those who responded may not have been representative of the entire group, since people who gain back large amounts of weight are generally unlikely to show up for follow-up tests, Mann said.

"Several studies indicate that dieting is actually a consistent predictor of future weight gain," said Janet Tomiyama, a UCLA graduate student of psychology and co-author of the study. One study found that both men and women who participated in formal weight-loss programs gained significantly more weight over a two-year period than those who had not participated in a weight-loss program, she said.

Another study, which examined a variety of lifestyle factors and their relationship to changes in weight in more than 19,000 healthy older men over a four-year period, found that "one of the best predictors of weight gain over the four years was having lost weight on a diet at some point during the years before the study started," Tomiyama said. In several studies, people in control groups who did not diet were not that much worse off — and in many cases were better off — than those who did diet, she said.

If dieting doesn't work, what does?

"Eating in moderation is a good idea for everybody, and so is regular exercise," Mann said. "That is not what we looked at in this study. Exercise may well be the key factor leading to sustained weight loss. Studies consistently find that people who reported the most exercise also had the most weight loss."

Diet studies of less than two years are too short to show whether dieters have regained the weight they lost, Mann said.

"Even when you follow dieters four years, they're still regaining weight," she said.

One study of dieting obese patients followed them for varying lengths of time. Among those who were followed for fewer than two years, 23 percent gained back more weight than they had lost, while of those who were followed for at least two years, 83 percent gained back more weight than they had lost, Mann said. One study found that 50 percent of dieters weighed more than 11 pounds over their starting weight five years after the diet, she said.

Evidence suggests that repeatedly losing and gaining weight is linked to cardiovascular disease, stroke, diabetes and altered immune function. Mann and Tomiyama recommend that more research be conducted on the health effects of losing and gaining weight, noting that scientists do not fully understand how such weight cycling leads to adverse health effects.

Mann notes that her mother has tried different diets, and has not succeeded in keeping the weight off. "My mother has been on diets and says what we are saying is obvious," she said.

While the researchers analyzed 31 dieting studies, they have not evaluated specific diets.
Medicare raised the issue of whether obesity is an illness, deleting the words "Obesity is not considered an illness" from its coverage regulations in 2004. The move may open the door for Medicare to consider funding treatments for obesity, Mann noted.

"Diets are not effective in treating obesity," said Mann. "We are recommending that Medicare should not fund weight-loss programs as a treatment for obesity. The benefits of dieting are too small and the potential harm is too large for dieting to be recommended as a safe, effective treatment for obesity."

From 1980 to 2000, the percentage of Americans who were obese more than doubled, from 15 percent to 31 percent of the population, Mann noted.

A social psychologist, Mann, taught a UCLA graduate seminar on the psychology of eating four years ago. She and her students continued the research when the course ended. Mann's co-authors are Erika Westling, Ann-Marie Lew, Barbra Samuels and Jason Chatman.

"We asked what evidence is there that dieting works in the long term, and found that the evidence shows the opposite" Tomiyama said.

The research was partially supported by the National Institute of Mental Health.

In future research, Mann is interested in studying whether a combination of diet and exercise is more effective than exercise alone.

UCLA is California's largest university, with an enrollment of nearly 37,000 undergraduate and graduate students. The UCLA College of Letters and Science and the university's 11 professional schools feature renowned faculty and offer more than 300 degree programs and majors. UCLA is a national and international leader in the breadth and quality of its academic, research, health care, cultural, continuing education and athletic programs. Four alumni and five faculty have been awarded the Nobel Prize.

Before drawing a conclusion that Diets are negative because they cause Weight-Gain,
it is important to remember that there is a Difference between Causation and Correlation.
See Linked article.

Just because Fat People and Dieting are Associated,
doesn’t mean that Dieting Causes People to be fat.

For the past eight-and-a-half years I’ve entered all of my daily food into a computer program that tells me the micronutrients in that food, including calories. The computer program that I choose to use is called DietPower.

I’ve written quite a lot about calories, including the impossibility of achieving a totally accurate calorie count. Below are links to two of those articles:

Do Calories Matter?

Calorie Detective – Lying Food Labels

A calorie is simply a measurement of energy, the amount of heat that something gives off through chemical processes. This is an “inexact” scientific concept which has been simplified for general use. Although there is nothing “perfectly accurate” about a calorie measurement, at this time there doesn’t appear to be an alternative way for Science to better measure the potential energy which is contained inside foods.

For me, “counting calories” is personally helpful as a “general” measuring tool,
while understanding that:

• All bodies are not the same.
  
  
• It is important not to put too much Faith into the exact calorie numbers that “Experts” SAY one’s body burns.
  
  
• It is important not to put too much Faith into the exact calorie numbers allegedly contained in any food item.

Even though it is true that our bodies process different macronutrients differently, … at the end of the day… it still remains that if a body consumes more energy than a body expends, it will accumulate fat.

The article below states the Paleo / Low-Carb position against using calories as a food measurement tool, which is basically: “The concept of the “calorie”, as applied to nutrition, is an oversimplification so extreme as to be untrue in practice.”

There Is No Such Thing As A “Calorie” (To Your Body)
           by J. Stanton, online Paleo blogger, 
                author of The Gnoll Credo (2010)  (science fiction fantasy about primitive man)

A friend of mine once said “The problem with explaining complicated systems to the layman is this: it’s easy to simplify a concept to the point that that it’s no longer true.”

To that end, I submit the following hypothesis:

The concept of the “calorie”, as applied to nutrition, is an oversimplification so extreme as to be untrue in practice.

What Is A “Calorie”, Anyway?

The dietary calorie is defined as “the amount of energy required to increase the temperature of 1 kilogram of water by 1 degree Kelvin.”

The dietary calorie is actually a “kilocalorie” = 1000 calories, which is why you’ll occasionally see it abbreviated as “kcal”.

It’s an obsolete unit: the “joule” is the modern unit of energy. There are 4.184 joules in a calorie, and 4184 in a dietary calorie (kilocalorie).

Problem: Our Bodies Don’t Use “Calories”

You may already see the problem here: a “calorie” is a unit of energy transfer. We determine the number of “calories” in a food by, quite literally, burning it and measuring how much heat it generates.

This is a bomb calorimeter. Note: not equivalent to the human digestive and metabolic system.

Unfortunately, our bodies are not steam engines! They do not burn the food we eat in a fire and convert the heat into mechanical work. Thus:

There is no biochemical system in our bodies whose input is a “calorie”.

Every metabolic pathway in our body starts with a specific molecule (or family of molecules), and converts it into another molecule—usually consuming energy in the process, not producing it.

This is why we must eat food in order to stay alive. The chemical reactions that build and repair each one of the trillions of cells in our bodies, from brain to toe, from eye to pancreas, require both energy and raw materials. The chemical reactions that allow our cells to perform their necessary functions, from transporting oxygen to parsing visual input to generating muscular force to manufacturing mucus and bile and stomach acid and insulin and leptin and T3, require both energy and raw materials. And the chemical reactions that allow our cells to communicate, via hormones and neurotransmitters, require both energy and raw materials.

In summary, the food we eat has many possible fates. Here are the major ones:

• Food can be used to build and repair our tissues, both cellular (e.g. muscles, skin, nerves) and acellular (e.g. hair, collagen, bone mineral).
  
  
• It can be used to build enzymes, cofactors, hormones, and other molecules necessary for cellular function and communication.
  
  
• It can be used to build bile, stomach acid, mucus, and other necessary secretions, both internal and external.
  
  
• It can be used by gut bacteria to keep themselves alive, and the waste products of its metabolism can meet any of the other fates listed here.
  
  
• It can fail to be digested or absorbed, and be excreted partially or completely unused.
  
  
• It can be converted to a form in which it can be stored for future use, such as glycogen or fat.
  
  
• It can be transported to an individual cell that takes it in, and converts it to energy, in order to perform the above tasks.

Note that only the last of these fates—immediate conversion to energy—even approximates the definition of a dietary “calorie”.

Why “Calories In, Calories Out” Is A Radical Oversimplification

By now, the problem with “calories in, calories out” should be obvious:

The fate of a “calorie” of food depends completely on its specific molecular composition, the composition of the foods accompanying it, and how those molecules interact with our current metabolic and nutritional state.

Note that “our current metabolic and nutritional state” is the definition of satiety, as I explain in my ongoing article series “Why Are We Hungry?”, and in my 2012 AHS presentation.

Did you just have an epiphany? I hope so.

So What Matters, If Not “Calories”?

Of the possible fates I listed above, only one is wholly undesirable…storage as fat.

I speak from the modern, First World point of view, in which obesity and the metabolic syndrome are more common health problems than starvation.

And while space does not permit a full exploration of all the possible fates of an ingested “calorie” (it’s called a “biochemistry textbook”), I will give a few examples.

A Few Possible Fates Of A “Calorie”: Protein

Imagine a molecule of “protein”.

Proteins are made up of chains of amino acids. (Learn more about proteins and their structure here.) Some proteins, such as meat, are readily digested and absorbed. Some are poorly digestible, such as the prolamins found in grains like wheat and corn, and part of them will either feed gut bacteria or be excreted. Then, once protein is absorbed, its composition of amino acids determines how much of the protein we can use to build and repair (the first three fates in the list above), and how much must be burned for energy or excreted.

The amino acid composition of grains is different than what our bodies need, since the metabolic needs of a grass seed are very different than the metabolic needs of a human being. That’s why grains score so low on measures of protein quality, such as the PDCAAS, compared to meat and eggs. (Grains score 0.25-0.4, versus approximately 1.0 for all animal-source proteins.)

But even if the protein is perfectly digested, absorbed, and of high quality, that is no guarantee of its fate! If we’ve already absorbed enough complete protein for our body’s needs, additional protein will still be converted to glucose, burned for energy, or excreted, no matter how high its quality. (Our bodies have no dedicated storage reservoir for protein…the process of muscle-building is very slow, and only occurs when stimulated by the right kinds of exercise.)

So, right away we can see that a “calorie” of meat protein that is digested, absorbed, and used to build or repair our bodies is not equal to a “calorie” of meat protein surplus to our needs. Nor is it equal to a “calorie” of wheat protein that is only partially digested, poorly absorbed, and disruptive to the digestive tract itself! (e.g. Fasano 2011)

A Few Possible Fates Of A “Calorie”: Fructose

(Again, space does not permit a full exploration of all possible fates of all possible types of “calories”, so these explanations will be somewhat simplified.)

Imagine a molecule of fructose.

Under ideal conditions, fructose is shunted immediately to the liver, where it is converted into glycogen and stored for future use. However, fructose has many other possible fates, all bad. It can fail to be absorbed, whereupon it will feed gut bacteria—a process that can cause SIBO, and consequent acid reflux, when continued to excess. If our liver is already full of glycogen, fructose is converted to fat—a process strongly implicated in NAFLD and visceral obesity. And when our liver is overloaded with fructose (or alcohol, which uses part of the same metabolic pathway), it can remain in circulation, where it can react with proteins or fats to form AGEs (advanced glycation endproducts), useless and/or toxic pro-inflammatory molecules which must be filtered out by the liver.

A typical Big Gulp contains over 100 grams of HFCS. Even the typical “healthy” fruit smoothie contains over 90 grams of high-fructose fruit sugar!

An adult liver can only store, at most, 100-120g of glycogen…and our bodies never let it become deeply depleted.

The problem here should be obvious.

Now ask yourself: which of the above fates has any meaning relative to the definition of a “calorie”?

A Few Possible Fates Of A “Calorie”: Starch

I can’t possibly explore all the fates of starch, but here are some common ones.

Starch is made of glucose molecules chained together. Upon digestion, it’s broken down into these individual glucose molecules, and absorbed—usually reasonably well, unlike fructose (though certain forms, called “resistant starch”, are indigestible and end up being used for energy by our gut bacteria).

Once glucose enters our bloodstream, its fate depends on a host of metabolic and nutritional factors. Ideally, because high blood glucose is toxic, our muscles and liver are not already full of glycogen, and insulin will quickly force it into one of them, whereupon it will be stored as glycogen and used as needed. Our brain and red blood cells also need glucose, since they can’t run on fat, and if they’re low on energy they can burn it too.

Unfortunately, as we’ve seen, our liver has a very small storage capacity, and the capacity of our muscles isn’t very large either—1-2% of muscle mass.

A 155 pound (70 kilo) adult at 14% bodyfat will contain about 66 pounds (30 kg) of muscle, leaving him with 300-600 grams of glycogen storage, depending on his level of training. (Source.)

Note that only reasonably intense exercise (> 50% VO2max) significantly depletes muscle glycogen, and only from the muscles used to perform the effort. Also note that the mainstream recommendation of 50-60% of daily “calories” from carbohydrate equals 300g-360g for a 2400 “calorie” diet.

Again, the problem here should be obvious.

Then, our cells will try to switch over to burning the surplus of available glucose, instead of burning fat for energy.

People with impaired metabolic flexibility have a problem switching between glucose and fat metabolism, for reasons that are still being investigated.

This is yet another example of how our nutritional and metabolic state affects the fate of a “calorie”; why a “calorie” of fat and a “calorie” of sugar are not equivalent in any sane sense of the word; and why different people respond differently to the same number and composition of “calories”.

Next, our body will try to “rev up” our basal metabolic rate in order to burn off the excess glucose…if sufficient cofactors such as T3 are available, and if our metabolic flexibility isn’t impaired. And a continued surplus will be (slowly) converted to fat in either the liver or in fat cells…but if it remains in circulation, it can react with proteins or fats to form AGEs (though more slowly than fructose).

Note that these proteins and fats can be part of living tissues: neuropathy, blindness, and all the complications of diabetes are consequences of excessively high blood sugar over the long term.

Are you starting to understand why the concept of a “calorie” is so oversimplified as to be effectively meaningless?

A Few Possible Fates Of A “Calorie”: Fat

Explaining all possible fates of all possible fats, even cursorily, would require an even longer section than the above two! However, I trust my point is clear: the fate of dietary linoleic acid differs from the the fate of DHA, the fate of palmitic acid, or the fate of butyrate, and their effects on our nutritional and metabolic state will also differ.

But Wait, There’s More

I also don’t have time or space to explore the following important factors:

• Energy loss when food is converted to different forms of storage (e.g. gluconeogenesis, glycogenesis, lipogenesis) or retrieved from storage
  
  
• How different types and quantities of dietary protein, fat, and carbohydrate affect our hormonal and metabolic environment
  
  
• How the fate of a “calorie” depends on the composition of the other foods it’s eaten with
  
  
• How different types and quantities of food, as well as our nutritional and metabolic state (our satiety), affect our perception of hunger
  
  
• The host of known, measurable differences between individuals, such as MTHFR genes, the respiratory quotient, and the bewildering variety of hormones on the HPTA axis.

Conclusion: The Concept Of A “Calorie” Is So Oversimplified As To Be Meaningless

Let’s recap some of the possible fates of a “calorie”:

• Food can be used to build and repair our tissues, both cellular (e.g. muscles, skin, nerves) and acellular (e.g. hair, collagen, bone mineral).
  
  
• It can be used to build enzymes, cofactors, hormones, and other molecules necessary for cellular function and communication.
  
  
• It can be used to build bile, stomach acid, mucus, and other necessary secretions, both internal and external.
  
  
• It can be used by gut bacteria to keep themselves alive, and the waste products of its metabolism can meet any of the other fates listed here.
  
  
• It can fail to be digested or absorbed, and be excreted partially or completely unused.
  
  
• It can be converted to a form in which it can be stored for future use, such as glycogen or fat.
  
  
• It can be transported to an individual cell that takes it in, and converts it to energy, in order to perform the above tasks.

Note that only the last of these fates—immediate conversion to energy—even approximates the definition of a dietary “calorie”.

I hope it is now clear that the fate of a “calorie” depends on a bewildering host of factors, including our current nutritional and metabolic state (our satiety), the composition of the other foods it’s eaten with; our biochemical individuality, both genetic and environmental; and much more.

Takeaways

• There is no biochemical system in our bodies whose input is a “calorie”.
  
  

• The food we eat has many possible fates, only one of which approximates the definition of a dietary “calorie”.
  

• The fate of a “calorie” of food depends completely on its specific molecular composition, the composition of the foods accompanying it, and how those molecules interact with our current metabolic and nutritional state—our satiety.
  

• Therefore, the concept of the “calorie”, as applied to nutrition, is an oversimplification so extreme as to be untrue in practice.
  

• Therefore, the concept of “calories in, calories out”, or CICO, is also unhelpful in practice.
  

• The health-supporting fates of food involve being used as raw materials to build and repair tissues; to build enzymes, cofactors, and hormones; to build bile, mucus, and other necessary secretions; to support “good” gut bacteria, while discouraging “bad” bacteria; and, once all those needs are taken care of, providing energy sufficient to perform those tasks (but no more).
  

• Therefore, we should eat foods which are made of the raw materials we need to perform and support the above functions.

• Biochemical individuality means that the optimum diet for different people will differ—as will their tolerance for suboptimal diets.

• However, eating like a predator—a diet based on meat, fish, shellfish, vegetables and fruit in season, and just enough starch to support your level of physical activity—is an excellent starting point.

The author of this article is J. Stanton, who is an online Paleo blogger, and the author of The Gnoll Credo (2010) which is a science fiction fantasy about primitive man.

I've been unable to discover information about J. Stanton’s education or any indication that he has any professional credentials. At present, no bio exists on his blog, and his biography as posted on Amazon is quoted below:

"J. Stanton has written and published home and arcade video games, rock, electronic, and tribal music, automobile reviews, US and foreign patents, business plans, political campaign websites, and advertising copy. He spends much of his time ascending and descending mountains on skis, on bicycles, and on foot."

 I’ve enjoyed reading past nutritional articles in J. Stanton’s blog at www gnolls.org, and a year or so ago I got his book, The Gnoll Credo (2010) from Amazon. Although I do read a great many books, enjoy reading, and have read lots of science fiction, this book did not hold my interest. I’ve not yet been able to force myself to read beyond the first few pages. Perhaps I’m too civilized or perhaps the plot is too much of a “boy” thing for me. However, I do own the book, and someday, I might choose to finish reading it.

 
What about eating frequency? How often should we eat?

Should we eat 3 Square Meals?

Or should we eat 6 Small Meals?

Or should we eat only inside a window of 8 hours or 5 hours?

Or should we, intermittently, have days with only one small meal, or even zero food in a total water fast?

Or should we eat whenever we feel Hunger?

Each of these “Diets”, “Non-Diets”, “Ways-of-Eating”, or “Lifestyles” claims that Scientific Research supports their individual position.

So what DO we do?
The following article by Dr. Yoni Freedhoff of WeightyMatters, supports my own personal position on this question.

Does New Study settle the
3 Square vs. 6 Small vs. the 8 hr Diet Debate?

So this month yet another study in a never-ending line of studies looking to compare the impact of meal frequency on fullness and biochemistry came out. This one suggested that small frequent helped decrease energy intake in normal weight men.

Honestly I pretty much disregard all of these studies.

Not because I'm doubting or questioning their results, just that I don't think their results really matter.

What I mean is that all of these studies fail to address the practical aspects of living with their recommendations, and as a clinician, that's really all that matters to me.

I've seen people controlling calories, loving life and preserving health with 6 small meals daily. I've seen people do the same on 2, 3, 4, and in some cases even 1 meal a day.

Regardless of the research that comes out, what matters more than what a physiology paper says is how you personally feel.

In my office we do tend to start people on small and frequent meals and snacks. But if that doesn't suit or help the individual we'll shift to 3 square meals. We've also recommended the intermittent fasting style that's suddenly finding some traction on the diet book shelves.

You need to find a life that you enjoy, and just because a new study or diet book suggests there's a "better", or "right", way, if you don't happen to enjoy it, it just isn't going to work.

The specific new study referred to is: Psychology and Behavior
www. sciencedirect.com/science/article/pii/S0031938413000243

According to all of the scientific research I’ve read, when we get right down to it, any actual “Health” or “Metabolic” Benefit Differences between all of these eating plans are truly miniscule, and therefore, not even worth the individual effort of personal consideration. The question to consider is which one can we DO?

I ask myself:

• Which Eating Behavior will work for ME in MY weight-loss or maintenance efforts?.
  
• Which Behavior will allow ME to consistently eat less than, or the same as, the amount that My body uses for energy?
  
• Is one Eating Behavior more manageable for ME than another?
  
• Which one can I consistently stay on?
  
• Can I live with one of these Behaviors as a lifetime Habit?

I recently posted an article: Do Calories matter ... discussing this issue with regard to Low-Carb eating.  Here is a Paleo expert's recently stated viewpoint on whether or not Calories matter.

Low Carb and Paleo: My Thoughts Part 1
                    By Rob Wolf

Slowly I realized, both by experimentation and by really looking at the literature: CALORIES MATTERED MORE THAN CARBS FOR BODY-COMP.

I have to say this was a pretty big shake-up for me. I’d assumed one could eat as much fat as one desired and STILL get leaner. As I mentioned above, when I first started eating Low Carb, or more specifically, cyclic low carb (CLC) I was leaner than ever in my life. I know based on blood work and fat deposition that I had insulin resistance while vegan, and CLC helped with this immensely, but it was my new-found energy and activity level that drove my leanness, not an inability to store fat in the absence of significant insulin.

I think this is one of the most damaging messages that comes out of the Low Carb camp to this day, I was duped by this, so I’m not going to do what a lot of other recovered Low Carb writers do and make folks out to be idiots for still believing this…but, it is time to face facts. In every damn study it is clear that for fat loss we’d like adequate protein, and a calorie restriction scenario. Low Carb is fantastic for this in that one typically feels satisfied on high protein, moderate fat, loads of veggies. If one is insulin resistant, this approach can be nothing short of miraculous. HOWEVER! If one manages to cram enough cheese, olive oil and grass-fed butter down the pie-hole, this is in fact, a “mass gain” diet.

Low Carb is fantastic for the insulin resistant individual, as it addresses both glycemic load and satiety. But if one manages to bypass normal satiety mechanisms, or if one can find some combinations of highly palatable, but low-carb foods, it’s still a ticket to Fat Camp.

The insistence on the part of the Low Carb community in adhering to the “no insulin, no fat gain” dogma ends up discrediting the real therapeutic benefit of Low Carb and hurts us all. The insulin resistant, crack-addicted individual really benefits from Low Carb, I cannot say that sufficiently, and the ease with which people lose weight (fat) on these programs is remarkable, but insulin control takes a backseat to calorie reduction via highly satiating foods. This whole situation further damages the ability to push ketosis as a therapeutic treatment for everything from cancer to neurodegenerative disease. It’s a tool folks, not an end-all-be-all.”

  ROBB WOLF is a former research biochemist and is regarded as one of the world's leading experts in Paleolithic nutrition.  He authored the best-selling book: The Paleo Solution (2010). Other books by him are: Practical Paleo (2012); Paleo Slow Cooking (2012); Paleo Comfort Foods (2011); Everyday Paleo (2011).

Wolf is a former California State Powerlifting Champion (565Lb Squat, 345lb Bench, 565lb Dead Lift) and a 6-0 amateur kickboxer. He coaches athletes at the highest levels of competition and consults with Olympians and world champions in MMA, motocross, rowing and triathlon.