Interesting Studies: Probably low carb related in one way or another

Separate circuitries encode the hedonic and nutritional values of sugar

Mice study: Biological effects of sugar more important than taste.

Abstract

Sugar exerts its potent reinforcing effects via both gustatory and post-ingestive pathways. It is, however, unknown whether sweetness and nutritional signals engage segregated brain networks to motivate ingestion. We found in mice that separate basal ganglia circuitries mediated the hedonic and nutritional actions of sugar. During sugar intake, suppressing hedonic value inhibited dopamine release in ventral, but not dorsal, striatum, whereas suppressing nutritional value inhibited dopamine release in dorsal, but not ventral, striatum. Consistently, cell-specific ablation of dopamine-excitable cells in dorsal, but not ventral, striatum inhibited sugar's ability to drive the ingestion of unpalatable solutions. Conversely, optogenetic stimulation of dopamine-excitable cells in dorsal, but not ventral, striatum substituted for sugar in its ability to drive the ingestion of unpalatable solutions. Our data indicate that sugar recruits a distributed dopamine-excitable striatal circuitry that acts to prioritize energy-seeking over taste quality.

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Source for the above 2006 article.

Effects of Twenty Days of the Ketogenic Diet on Metabolic and Respiratory Parameters in Healthy Subjects.

METHODS:

Thirty-two healthy subjects were randomized into two groups. The KD group followed a ketogenic diet for 20 days (KD t 0-t 20), then switched to a low-carbohydrate, no-ketogenic diet for 20 days (KD t 20-t 40), and finally was on a Mediterranean diet (MD) for 2 more months (KD t 40-t 2m). The MD group followed a MD for 20 days (MD t 0-t 20), then followed a MD of 1400 kcal over the next 20 days (MD t 20-t 40), and completed the study with the MD for 2 months (MD t 40-t 2m). Body weight, body fat, respiratory rate, and respiratory gas parameters (including respiratory exchange ratio (RER) and carbon dioxide end-tidal partial pressure (PETCO2), oxygen uptake (VO2), carbon dioxide production (VCO2), and resting energy expenditure (REE)) were measured at each point.

RESULTS:

A significant decrease (p < 0.05) in RER was observed after 20 and 40 days in the KD group, but not in the MD group. In the KD group, significant reductions were observed for both carbon dioxide output and PETCO2, however, there was no significant change in VO2, VCO2, and REE. While both diets significantly decreased body fat mass, the KD diet overall proved to have a higher percentage of fat loss versus the MD diet.

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Disruption of the sugar sensing receptor T1R2 attenuates metabolic derangements associated with diet-induced obesity.

Mouse study.

We assessed body composition, energy balance, glucose homeostasis and tissue-specific nutrient metabolism in T1R2 knock-out (T1R2-KO) mice fed a HF/LC diet for 12-weeks. HF/LC diet fed T1R2-KO mice gained a similar amount of body mass as WT mice, but have reduced fat mass and increased lean mass relative to WT mice. T1R2-KO mice are also hyperphagic and hyperactive. Ablation of the T1R2 sugar sensor protected mice from HF/LC diet-induced hyperinsulinemia and altered substrate utilization, including increased rates of glucose oxidation and decreased liver triglyceride (TG) accumulation, despite normal intestinal fat absorption. Finally, STRs (T1r2/T1r3) are upregulated in the adipose tissue of WT mice in response to HF/LC diet and their expression positively correlates with fat mass and glucose intolerance.

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Impact of a ketogenic diet intervention during radiotherapy on body composition: I. Initial clinical experience with six prospectively studied patients


Background
Based on promising preclinical data, ketogenic diets (KDs) have been proposed as supplementary measures for cancer patients undergoing standard-of-care therapy. However, data is still scarce on the tolerability and effects of KDs on cancer patients undergoing radiotherapy (RT). Here we present six cases of patients who underwent RT and concurrently consumed a self-administered KD in our clinic within a busy community hospital setting.

Methods
All patients were followed prospectively with measurements of blood parameters, quality of life and body weight and composition using bioelectrical impedance analysis.

Results
No adverse diet-related side effects occurred. Two patients had no elevated ketone body levels in serum despite self-reporting compliance to the diet. There was consensus that the KD was satiating and weight loss occurred in all patients, although this was only significant in two patients. Our data indicate that weight loss was mainly due to fat mass loss with concurrent preservation of muscle mass. Overall quality of life remained fairly stable, and all subjects reported feeling good on the diet. Tumor regression occurred as expected in five patients with early stage disease; however one subject with metastatic small cell lung cancer experienced slight progression during three cycles of combined chemotherapy + KD and progressed rapidly after ending the KD.

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The Latest on Low-Carb, High-Fat Diets
By: Alex Hutchinson

A nice summary of the science on whether it’s possible, or even preferable, to compete as a high-level endurance athlete on a LCHF diet.

Research mentioned in the article:

• Fat adaptation followed by carbohydrate loading compromises high-intensity sprint performance. (2006)
• Metabolic characteristics of keto-adapted ultra-endurance runners. (2016)
• Enhanced Endurance Performance by Periodization of CHO Intake: "Sleep Low" Strategy. (2016)

And a great companion blog post by Evan Dunfee who participated in the study and a few weeks later "notched a huge personal best at a 50-kilometer race in Australia, smashing the Canadian record and punching his ticket to the Rio Olympics this summer."

A Cracking Start to 2016...

Long-term effects of a very low carbohydrate weight loss diet and an isocaloric low-fat diet on bone health in obese adults

Conclusion

Weight loss following a hypocaloric LC diet compared with an LF diet does not differentially affect markers of bone health over 12 months in overweight and obese adults.

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Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)

Conclusions Available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. Findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.

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Blog Posts

I like Dr. Malcom Kendrick's summary of the findings from his blog post, Greater Cholesterol lowering increases the risk of death:

THE MORE THE CHOLESTEROL WAS LOWERED THE GREATER THE RISK OF DEATH

The Minnesota Coronary Experiment (MCE), a randomized controlled trial conducted in 1968-73, was the largest (n=9570) and perhaps the most rigorously executed dietary trial of cholesterol lowering by replacement of saturated fat with vegetable oil rich in linoleic acid. The MCE is the only such randomized controlled trial to complete post-mortem assessment of coronary, aortic, and cerebrovascular atherosclerosis grade and infarct status and the only one to test the clinical effects of increasing linoleic acid in large prespecified subgroups of women and older adults.

And Tom Naughton is always an entertaining read. His take: Another Big Fat Fail For The Lipid Hypothesis

Consumption of Honey, Sucrose, and High-Fructose Corn Syrup Produces Similar Metabolic Effects in Glucose-Tolerant and -Intolerant Individuals

Conclusions: Daily intake of 50 g carbohydrate from honey, sucrose, or HFCS55 for 14 d resulted in similar effects on measures of glycemia, lipid metabolism, and inflammation. All 3 increased triglyceride (TG) concentrations in both glucose tolerance (GT) and impaired glucose tolerance (IGT) individuals and elevated glycemic and inflammatory responses in the latter.

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50g of added sugar daily for two weeks was enough to negatively impact health markers.

AlabasterVerve wrote: »

The long read
The sugar conspiracy
by Ian Leslie

Not a study but an interesting read.

In 1972, a British scientist sounded the alarm that sugar – and not fat – was the greatest danger to our health. But his findings were ridiculed and his reputation ruined. How did the world’s top nutrition scientists get it so wrong for so long?

Guardian Article

Yale Daily News on Dr. Katz (regarding the article above):

Instructor criticized for comments

The first results from NuSi's metabolic ward study were shared at ICO 2016 by Kevin Hall. In a nut shell his findings were there's no metabolic advantage to a ketogenic diet; there may be something interesting going on with appetite.

Here's a short 13 minute interview of Kevin Hall at the conference by Yoni Freedhoff:

Dr. Kevin Hall on NuSi first public presentation of their metabolic ears work.

Conclusions:

1. An inpatient controlled isocaloric low carbohydrate ketogenic diet was
followed by small increases in energy expenditure that waned over time.

2. Despite rapid, substantial and persistent reductions in insulin
secretion (as assessed by 24hr C-peptide excretion) and RQ, no
augmentation of body fat loss was observed.

3. Our data do not support the carbohydrate insulin model predictions of
physiologically significant increases in energy expenditure or body fat
loss in response to an isocaloric low carbohydrate ketogenic diet.

Some of the Q&A with Yoni Freedhoff and Kevin Hall:

Q: I take it this has not increased your buy in for the insulin hypothesis?
A: I think the combination of these two studies - on the metabolic side of things - basically falsify the carbohydrate insulin hypothesis.

Q: When's the paper coming out?
A: It was just resubmitted to the American Journal of Clinical Nutrition after a round of relatively positive reviews. So I would anticipate probably hearing something positive within the next few weeks.

Q: Does this mean the hypothesis is now over? I suspect you would say yes.
A: I still think there might be something interesting to say about appetite. [Appetite] was something that was measured very indirectly in this study which I'm not presenting the data yet.

Insulin decreases atherosclerosis by inducing endothelin receptor B expression

Mice study: Improved insulin signaling reduces atherosclerosis in mouse models

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