Interesting Studies: Probably low carb related in one way or another
AlabasterVerve
Posts: 3,171 Member
I read a lot of nutrition news, studies, blogs and what not and may mention something I've read when I post. I have no interest in "proving" anything I say but for those genuinely interested in the topic I thought I start a thread to post links as I come across studies I find interesting in some way.
The association between dietary saturated fatty acids and ischemic heart disease depends on the type and source of fatty acid in the European Prospective Investigation into Cancer and Nutrition–Netherlands cohort
CONCLUSIONS:
In this Dutch population, higher SFA intake was not associated with higher IHD risks. The lower IHD risk observed did not depend on the substituting macronutrient but appeared to be driven mainly by the sums of butyric through capric acid, the sum of pentadecylic and margaric acid, myristic acid, and SFAs from dairy sources. Residual confounding by cholesterol-lowering therapy and trans fat or limited variation in SFA and PUFA intake may explain our findings. Analyses need to be repeated in populations with larger differences in SFA intake and different SFA food sources.
Source
The association between dietary saturated fatty acids and ischemic heart disease depends on the type and source of fatty acid in the European Prospective Investigation into Cancer and Nutrition–Netherlands cohort
CONCLUSIONS:
In this Dutch population, higher SFA intake was not associated with higher IHD risks. The lower IHD risk observed did not depend on the substituting macronutrient but appeared to be driven mainly by the sums of butyric through capric acid, the sum of pentadecylic and margaric acid, myristic acid, and SFAs from dairy sources. Residual confounding by cholesterol-lowering therapy and trans fat or limited variation in SFA and PUFA intake may explain our findings. Analyses need to be repeated in populations with larger differences in SFA intake and different SFA food sources.
Source
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Higher compared with lower dietary protein during an energy deficit combined with intense exercise promotes greater lean mass gain and fat mass loss: a randomized trial
Conclusions: Our results showed that, during a marked energy deficit, consumption of a diet containing 2.4 g protein · kg−1 · d−1 was more effective than consumption of a diet containing 1.2 g protein · kg−1 · d−1 in promoting increases in LBM and losses of fat mass when combined with a high volume of resistance and anaerobic exercise. Changes in serum cortisol were associated with changes in body fat and LBM, but did not explain much variance in either measure.
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Comparison of the DASH (Dietary Approaches to Stop Hypertension) diet and a higher-fat DASH diet on blood pressure and lipids and lipoproteins: a randomized controlled trial.
CONCLUSIONS:
The HF-DASH diet lowered blood pressure to the same extent as the DASH diet but also reduced plasma triglyceride and VLDL concentrations without significantly increasing LDL cholesterol.
Source8 -
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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One more for the thread: Ketosis leads to increased methylglyoxal production on the Atkins diet.
Abstract
In the popular and widely used Atkins diet, the body burns fat as its main fuel. This process produces ketosis and hence increased levels of beta-hydroxybutyrate (BOB) acetoacetate (AcAc) and its by-products acetone and acetol. These products are potential precursors of the glycotoxin methylglyoxal. Since methylglyoxal and its byproducts are recognized as a significant cause of blood vessel and tissue damage, we measured methylglyoxal, acetone, and acetol in subjects on the Atkins diet. We found that by 14-28 days, methylghyoxal levels rose 1.67-fold (P = 0.039) and acetol and acetone levels increased 2.7- and 6.12-fold, respectively (P = 0.012 and 0.028). Samples from subjects with ketosis showed even greater increases in methylglyoxal (2.12-fold), as well as acetol and acetone, which increased 4.19- and 7.9-fold, respectively; while no changes were seen in samples from noncompliant, nonketotic subjects. The increase in methylglyoxal implies that potential tissue and vascular damage can occur on the Atkins diet and should be considered when choosing a weight-loss program.
Source11 -
Source for the above 2006 article.1
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AlabasterVerve wrote: »Source for the above 2006 article.
Apologies, I thought I included the source link. Edited the post to include it.3 -
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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Insulin regulates hepatic triglyceride secretion and lipid content via signaling in the brain.
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AlabasterVerve wrote: »Source for the above 2006 article.
Full text is behind a $paywall but here's a bright guy's view of the above http://high-fat-nutrition.blogspot.co.uk/2009/11/methylglyoxal-on-atkins-uh-oh.html1 -
Can ketones compensate for deteriorating brain glucose uptake during aging? Implications for the risk and treatment of Alzheimer's disease.
Abstract
Brain glucose uptake is impaired in Alzheimer's disease (AD). A key question is whether cognitive decline can be delayed if this brain energy defect is at least partly corrected or bypassed early in the disease. The principal ketones (also called ketone bodies), β-hydroxybutyrate and acetoacetate, are the brain's main physiological alternative fuel to glucose. Three studies in mild-to-moderate AD have shown that, unlike with glucose, brain ketone uptake is not different from that in healthy age-matched controls. Published clinical trials demonstrate that increasing ketone availability to the brain via moderate nutritional ketosis has a modest beneficial effect on cognitive outcomes in mild-to-moderate AD and in mild cognitive impairment.
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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.
Source0 -
AlabasterVerve wrote: »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.
Source
Thats deep!0 -
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.
Source3 -
AlabasterVerve wrote: »Comparison of the DASH (Dietary Approaches to Stop Hypertension) diet and a higher-fat DASH diet on blood pressure and lipids and lipoproteins: a randomized controlled trial.
CONCLUSIONS:
The HF-DASH diet lowered blood pressure to the same extent as the DASH diet but also reduced plasma triglyceride and VLDL concentrations without significantly increasing LDL cholesterol.
Source
This one is interesting. Just passed it along to my husband since he has hypertension, high triglycerides and CAD.1 -
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...1 -
Digested wheat gluten inhibits binding between leptin and its receptor
Conclusions
Digested wheat gluten inhibits binding of leptin to the leptin receptor, with half-maximal inhibition at 10 ng/mL. The inhibition is significant at clinically relevant concentrations and could therefore serve as a novel pathway to investigate to understand the molecular basis of leptin resistance, obesity and associated disorders.
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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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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
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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.
Source
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 Hypothesis1 -
Harvard's response to those challenging the current saturated fat recommendations.
What would you say to those doubting the established guidelines surrounding the health benefits of replacing saturated fat with polyunsaturated fats as a result of this report? With this in mind, where should the research on dietary fats go next?
The bottom line is that this report adds no useful new information and is irrelevant to current dietary recommendations that emphasize replacing saturated fat with polyunsaturated fat, including sources of both n-3 and n-6 fatty acids. Many lines of evidence support this conclusion, including beneficial effects on blood lipids (6), summaries of prospective cohort studies (7), and randomized trials (8)—including the meta-analysis previously published by the authors in Ramsden et al. (5). Notably, since the 1960’s, the US diet has changed in this way; intake of linoleic acid has approximately doubled, and this has corresponded to a greater than 60 percent decline in coronary heart disease mortality (3). Although multiple factors have contributed to this decline, none of the other factors can explain this huge improvement in health, and the replacement of saturated fat with polyunsaturated fat (both n-6 and n-3 fatty acids) is almost certainly a major, probably most important, factor. Reversing these changes would almost certainly result in great harm.
Research Review: Old data on dietary fats in context with current recommendations
Nothing can explain the huge improvement in health other than a decrease in saturated fat? Nutrition "science" really is disgraceful.0
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