Tag Archives: carbohydrates

Carbs: Low vs. Lower

 

 

This was met with much backlash from the low carb cavalry, because, well, if low is good then lower must be better

I’m not anti-keto; but I’m not anti-science.  FACT.  

 

“…some people are not genetically equipped to thrive in prolonged nutritional ketosis.” –Peter Attia

  Continue reading

Share

Insulin, sympathetic nervous system, and nutrient timing.

Insulin secretion is attenuated by sympathetic nervous system activity; eg, via exercise.  Theoretically, exercising after a meal should blunt insulin secretion and I don’t think this will lessen the benefits of exercise, but rather enhance nutrient partitioning.   And this isn’t about the [mythical?] post-workout “anabolic window.”

Sympathetic innervation of pancreas: norepinephrine –> adrenergic receptor activation = decreased insulin secretion & increased lipolysis (Stich et al., 1999):

Stich insulin

Stich CAS

note how quickly catecholamines are cleared upon exercise cessation

Stich NEFA

Continue reading

Share

Insulin, dietary fat, and calories: context matters!

Jane Plain recently wrote a great article about the relationship between insulin, dietary fat, and calories.  There are a lot of data on this topic, which collectively suggest: context matters! 

For example,

Insulin and ketone responses to ingestion of MCTs and LCTs in man. (Pi-Sunyer et al., 1969)

14 healthy subjects, overnight fasted; dose: 1g/kg.

In brief, MCTs are more insulinogenic than corn oil.  But it’s not a lot of insulin.  Really.  Enough to inhibit lipolysis, perhaps, but that’s not saying much… & certainly not enough to induce hypoglycemia.

Pi-Sunyer MCT Corn oil

Continue reading

Share

Carbohydrates, calories, appetite, and body weight.

The Optimal Diet, Atkins, South Beach, Paleo, Zone… all have one thing in common: some degree of carbohydrate restriction.

Low, lower, lowest: does it matter?

There are 4 relatively large, randomized ‘diet-induced weight loss’ studies that all reported fairly comprehensive food intake and body composition data. The studies ranged in duration from 24 weeks to one year and included anywhere between 50 and ~300 overweight and obese participants.

In general, participants assigned to the low fat intervention were advised to restrict calories and fat whereas those assigned to low carb were told they could eat as much as they wanted as long as it wasn’t carbs.

Your mileage may vary – but these studies cover a large number of subjects from a wide range of backgrounds, suggesting the results might be applicable across the board.  Conclusion?  the amount of body fat lost was much more strongly associated with the reduction in carbohydrates than calories.  The only modestly surprising aspect was the magnitude… (see the figures below).

The four studies, in chronological order:

Brehm 2003: over the course of 6 months, those who consumed an average of 163 grams of carbohydrate per day lost 8.6 pounds of body weight while those who consumed 97 grams lost 18.7 pounds.

McAuley 2005: 24 weeks; those who ate 171 grams lost 10.3 pounds, while those who ate 133 grams lost 15.2 pounds, and those who ate 107 grams lost 15.6 pounds.

Maki 2007: 36 weeks; those who ate 186 grams lost 5.7 pounds, those who ate 131 grams lost 9.9 pounds.

Gardner 2007: 1 year – those who ate 138 grams lost 10.3 pounds, 181 grams lost 3.5 pounds, 195 grams lost 4.8 pounds, and 197 grams lost 5.7 pounds.

Continue reading

Share

Ketoacidosis

Nutritional ketosis is a normal, physiological response to carbohydrate and energy restriction.  A ketogenic diet is an effective weight loss strategy for many.  Ketoacidosis, on the other hand, is a pathological condition caused by insulin deficiency.  The common theme is low insulin; however, in ketoacidosis, blood glucose levels are very high.  Ketone levels are elevated in both states, although are 10-20x higher in ketoacidosis (~0.5-2 vs. > 20 mM).  Nutritional ketosis and ketoacidosis should not be confused with one another, and a ketogenic diet doesn’t cause ketoacidosis.

In ketoacidosis, gluconeogenesis occurs at a very high rate and the lack of insulin prevents glucose disposal in peripheral tissues.  Skeletal muscle protein breakdown contributes gluconeogenic substrates, exacerbating the problem.  This can cause blood glucose to reach pathological levels, exceeding 250 mg/dL.

Continue reading

Share

On resistant starch and blood glucose control

For overall health and well-being, fermented foods like sauerkraut and kefir are great.  Especially when following a low carbohydrate diet which is generally low in the types of foods which feed the gut microbiome.

For those with gastrointestinal problems, the gut microbiota is probably involved.  Whether it is bacterial overgrowth or dysbiosis, gut bugs are usually the culprit.  Treatment options vary widely, ranging from global extermination with vinegar & a low fibre diet (as per Jane Plain), or remodeling the microbiome with a prebiotic like galactooligosaccharides.   Probiotics like bifidobacteria can help, too, if they’re administered with either prebiotics or fermented foods (they need something to nourish them in transit).  Dark chocolate is also an excellent vessel.  Resistant starch is another option, although the question remains as to whether or not this is compatible with a low carbohydrate diet.

Resistant starch has been around for a while, and when I was in school it received about 10 minutes of attention during the fibre lecture.  But Jimmy Moore and Richard Nikolay have been talking about it a lot lately so I decided to freshen up on the topic.  In brief, it can be therapeutic for GI issues, but some studies have shown mixed effects on glucose & insulin metabolism.  The former is virtually unarguable, but I found the latter interesting.  And the impact of resistant starch on ketosis is included as well.

Continue reading

Share

Low carbohydrate diets favorably impact testosterone levels.

It is known.  Carbohydrate restriction improves (lowers) testosterone in women with PCOS.  It works for men, too… but by “works” I mean “increases.”

Decrease of serum total and free testosterone during a low-fat high fibre diet (Hamalainen et al., 1982) 

Intervention pseudo-crossover study: 30 healthy Finnish men in their 40’s were studied on their habitual high fat diet (40%  fat), then put on a low-fat (25%) high fibre diet for 6 weeks, then switched back to high fat.  The high fat diet was also higher in saturates, P:S ratio 0.15 vs. 1.25.

free T

 

Free testosterone levels declined on the low fat diet, but they recovered after 6 weeks of going back to their high [saturated] fat dieting (p < 0.01).

Some observational data: Testosterone and cortisol in relationship to dietary nutrients and resistance exercise (Volek et al., 1997)

…fat, and in particular saturated fat, is associated with increased testosterone levels [in men]:

observational

 

Continue reading

Share

Protein dilemma ~ sleepy or smart. #Gelatin

Gelatin and glycine have bounced around the blogosphere for quite some time.  Coming from a nutrition-centric place: you say gelatin, I think tryptophan (or lack thereof) and glycine.  Others think:

Jane Plain discusses positive mental effects of gelatin and pimps Pro-Stat (good source of glycine).  Chris Masterjohn discusses glycine and in typical WAP fashion seems to favor bone broth.  Knox gelatin didn’t help Michael Allen Smith sleep better, and he apparently tracks sleep quality quite well.  However, Sondra Rose thinks it improves sleep harmony, and gelatin simply blows Dana Carpender’s mind.

bones

Tryptophan-rich proteins like those found in whey and egg whites will elevate blood levels of tryptophan relative to other large neutral amino acids (Trp:LNAA ratio), leading to higher brain uptake and subsequent serotonin synthesis.  Tryptophan-poor proteins like gelatin do the opposite, and impair memory.  But the high glycine content in gelatin improves sleep quality.*  Glycine powder might be able to get around this, it’s dirt cheap and it seems to have the opposite effect on brain serotonin, albeit at a much higher dose (and in rats).

Continue reading

Share

Summer is fattening. Don’t do it in winter.

Seasonal eating proper

More from T.S. Wiley and Dr. Kruse on seasonal eating in what appears to be the primary model for its justification for use in humans – hibernating mammals.

How it goes, or so they say: in summer, hibernators massively overeat, including carb-rich foods, in order to generate muscle and liver insulin resistance, so as to promote body fat growth.  The long light cycle reduces evening melatonin, which pushes back the usual nighttime peak in prolactin, which causes an abnormal resistance to leptin, which induces hypothalamic NPY and subsequent carbohydrate craving.  Ergo, summer is fattening.  In today’s day, increased artificial lights guarantee year-round pseudo-summer; and we no longer experience the benefits of the short light cycle: longer sleep times (akin to hibernation) and fasting – either complete fasting as in hibernation, or pseudo-fasting, ie, a ketogenic diet.

Continue reading

Share

Silent Leptin Resistance

Conventional leptin resistance has something do with obesity.  It is known.  Silent leptin resistance is … err … complicated. 

Divide and conquer

Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding (Shapiro, Scarpace, et al., 2008 AJP)

A remarkable 60% fructose diet fed to rats for 6 months had absolutely no effect on energy balance.  Nil. QED.
Fig 1

Food intake and body weight were unaffected because the levels of and sensitivity to endogenous leptin were identical in both groups.

Enter the Dragon

Enter the Dragon

“Silent Leptin Resistance” – The fructose-fed rats are, however, profoundly resistant to the satiating effects of Metreleptin (a pharmaceutical grade injectable leptin analog):

Continue reading

Share