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High Fat? High Protein? Low Protein? What is really ketogenic?

The daily question that I get asked by my patients, and from those around the internet, relates to burning one’s own fat. “Don’t you have to limit the calories and limit fat you eat to burn your own body fat?

It seems everyone has a differing opinion on this question and a few of them have two opinions (you know who you are).  Very few of these opinions are grounded in the actual science of weight loss.

I hear coaches, trainers and even a number physicians argue, name call and rant about the need to cut calories to lose fat.  Yet, most of my patients “cut their calories” 200-1000 per day without successful fat reduction.  They may increase their exercise by 400-600 calories per day and still no weight loss.  This is the same crazy ineffective instruction we’ve been given for the last 50 years.

To be honest, there is a percentage of those in the fitness and modeling worlds upon which this dogma is effective and that is because of normal insulin levels and significant exercise. However, for the other 85% of the world who work over 40-80 hours a week, have children and families, serve in our churches and occasionally have a social life, myself included, it doesn’t work.  If we were all paid to exercise 2 hours a day and take “butt selfies” on Instagram, it might be easier.

Yes, you will probably lose 20 lbs. with calorie restriction, but your testosterone will drop by up to 50%, sex hormone binding globulin will double, and over time your basal metabolic rate will slow due to dramatic and often permeant reduction in thyroid function.  This makes it nearly impossible to lose more than that 20 lbs, and then you will regain the weight once calorie levels return to normal within 18-24 months.  (No one ever talks about that little problem, do they?)

For those of you that want to see success in weight loss, let’s outline a few essential principles that the trainers, keto-coaches and social media talking heads aren’t mentioning.

First, insulin has to be kept at a baseline.  The reason that 85% of people don’t, won’t and can’t see effective weight loss beyond 20-30 lbs long term (greater than 2 years) with calorie restriction is that 85% of the population has some degree of insulin resistance.  It’s not a disease, it’s a syndrome associated with the effect of the standard American diet.  I wrote a whole book about it called The Keto Cure.  We know that insulin and catecholamines increase the rate by which fat is stored.

Second, glucacon is a counter active hormone to keep your blood sugar from bottoming out.  The presence of glucagon stimulates fat burningIntermittent fasting and ketogenic dietary intake allow blood sugar to drop below 70 mg/dL (3.9 mmol/L) causing glucagon release and stimulate increased release of free fatty acids from the fat cells.

Third, two hormones, epinephrine and norepinephrine, are produced when blood sugar drops below 67 mg/dL (3.7 mmol/L).  Exercise lowers blood sugar to this level and stimulates additional burning of fat by engaging the release of glucagon and epinephrine and norepinephrine.  Exercise, also, has three other myokine hormonal effects making weight loss more successful when the diet is correctly balanced.

The fourth principle that is essential to understand relates to growth hormone.  Growth hormone stimulates and preserves muscle tissue, has a suppressive effect on insulin. Growth hormone increases with exercise, sleep, intermittent fasting and when protein intake is at least greater than 90 grams per day in women and around 1 gram of protein per body weight in men.  This is notably higher than previous calculations on protein that I have written about in the past.  Recent research, also found here, here and here, demonstrates that increased protein above 90-100 grams per day enhances muscle growth and stabilization and further suppresses insulin production beyond what we previously understood.
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Contrary to what the media has been saying about protein sources, not all protein is absorbed in the same way.  When it comes to absorption in the human gut and use by the human metabolism, protein sources differ in their effectiveness:

    • Egg protein utilization – 50%
    • Meat protein utilization – 40%
    • Cheese protein utilization 35-40%
    • Whey protein utilization – 18%
    • Vegetable protein utilization – 14%

Lastly, release of fat from the fat cell is mediated by natriuretic peptides and cGMP through the release of catecholamines, prostaglandins and nicotinic acid.  Interestingly, the major positive regulators of human lipolysis are catecholamines and natriuretic peptides (NPs). Fatty acid release from fat cells triples when catecholamines and natriuretic peptides are released.  Catecholamines are produced by exercise, stimulants and stress, and natriuretic peptides are stimulated by short change fatty acids (ketones).

For the science geeks in who follow my blog, I’ve included the following picture that summarizes the effects of these hormones on the fat cell.  The figure below shows the major pathways by which insulin, thyroid, catecholamines, testosterone and sympathomimetics effect fatty acid release from adipose tissue.

Primary signaling pathways in human lipolysis. Black and red lines indicate pro-lipolytic and anti-lipolytic signaling events, respectively. Arrows indicate stimulation and/or translocation and blunt lines indicate inhibition. Stimulation of lipolysis is dependent on PKA- or PKG-mediated phosphorylation of HSL and PLIN1. PKG is activated by cGMP, which is increased in response to activation of the GC-coupled NPR-A. Similarly, stimulation of the Gs-protein-coupled β1/2-ARs activates AC, which generates cAMP and activates PKA. Conversely, activation of Gi-protein-coupled α2-ARs inhibits AC and thereby reduces cAMP-dependent signaling to lipolysis. Stimulation of the insulin signaling pathway through the IR increases the activity of PDE3B, which converts cAMP to 5′-AMP, thus decreasing PKA activity and suppressing lipolysis. PKG activity is reduced by PDE5-mediated conversion of cGMP to 5′-GMP, although the upstream signals regulating this process are currently unknown. The dashed line indicates a putative Akt-independent insulin pathway acting selectively on PLIN1. α2-ARs, α2-adrenergic receptors; AC, adenylyl cyclase; TG, triglyceride; ATGL, adipose TG lipase; β1/2-ARs, β1- and β2-adrenergic receptors; CGI-58, comparative gene identification-58; DG, diacylglycerol; FFA, free fatty acid; GC, guanylyl cyclase; HSL, hormone-sensitive lipase; IR, insulin receptor; IRS1/2, IR substrates 1 and 2; MG, monoacylglycerol; MGL, monoglyceride lipase; NPR-A, type-A natriuretic peptide receptor; PDE3B, phosphodiesterase 3B; PDK, phosphoinositide-dependent kinase; PI3K, phosphatidylinositol 3-kinase; PKA, protein kinase A; PKB/Akt, protein kinase B; PLIN1, perilipin 1. (Journal of Molecular Endocrinology 52, 3; 10.1530/JME-13-0277)

The take home message from this information is this, effective long term weight loss cannot be achieved by calorie restriction.  Effective weight loss (specifically fat loss and muscle gain) is most effectively achieved when carbohydrates are restricted, protein is optimized, and proper exercise adequately triggers the release of fat burning hormones.

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I’d like to know, what combination has been most effective for you?

Have a great day!

Adam (eat your bacon) Nally, DO