Interesting Studies: Probably low carb related in one way or another
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Here's a blog post, A bread too far: Food structure and insulin responses, that relates to Kevin Hall's upcoming study on ultra processed foods. If the results of this study are reproduced there will be a difference between the ultra processed and the whole food diet.
Also relates to the sugar is sugar refrain that's so often repeated on MFP too - delivery method (aka food matrix) appears to matter which would go a long way to explaining peoples individual experiences with refined carbs. There was a food matrix study regarding homogenized milk a few years back that found similar differences I think? Either or, interesting stuff.
Re: Postprandial glucose, insulin, and incretin responses to grain products in healthy subjects.
CONCLUSIONS:
Postprandial insulin responses to grain products are determined by the form of food and botanical structure rather than by the amount of fiber or the type of cereal in the food. These effects may be mediated through GIP and GLP-1.
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Obesity Pathogenesis: An Endocrine Society Scientific Statement
Estimates suggest that in the United States obesity affects one-third of adults, accounts for up to one-third of total mortality, is concentrated among lower income groups, and increasingly affects children as well as adults. A lack of effective options for long-term weight reduction magnifies the enormity of this problem; individuals who successfully complete behavioral and dietary weight-loss programs eventually regain most of the lost weight.
We included evidence from basic science, clinical, and epidemiological literature to assess current knowledge regarding mechanisms underlying excess body-fat accumulation, the biological defense of excess fat mass, and the tendency for lost weight to be regained. A major area of emphasis is the science of energy homeostasis, the biological process that maintains weight stability by actively matching energy intake to energy expenditure over time.
Growing evidence suggests that obesity is a disorder of the energy homeostasis system, rather than simply arising from the passive accumulation of excess weight.
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AlabasterVerve wrote: »Here's a blog post, A bread too far: Food structure and insulin responses, that relates to Kevin Hall's upcoming study on ultra processed foods. If the results of this study are reproduced there will be a difference between the ultra processed and the whole food diet.
Also relates to the sugar is sugar refrain that's so often repeated on MFP too - delivery method (aka food matrix) appears to matter which would go a long way to explaining peoples individual experiences with refined carbs. There was a food matrix study regarding homogenized milk a few years back that found similar differences I think? Either or, interesting stuff.
Re: Postprandial glucose, insulin, and incretin responses to grain products in healthy subjects.
CONCLUSIONS:
Postprandial insulin responses to grain products are determined by the form of food and botanical structure rather than by the amount of fiber or the type of cereal in the food. These effects may be mediated through GIP and GLP-1.
Really interesting stuff... but I'm not a fan of a calorie is a calorie or a carb is a carb way of thinking though. I'm curious what Hull will find. And what he'll interpret those findings as meaning... I don't always agree with how he draws his conclusions.2 -
Insulin increases renal magnesium excretion: a possible cause of magnesium depletion in hyperinsulinaemic states.
physiological concentrations of insulin induce a specific increase in the renal excretion of magnesium. This might partly explain the magnesium depletion observed in various hyperinsulinaemic states, diabetes mellitus, atherosclerosis, hypertension, and obesity.
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Protein supplements after weight loss do not improve weight maintenance compared with recommended dietary protein intake despite beneficial effects on appetite sensation and energy expenditure: a randomized, controlled, double-blinded trial
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Blog post by Amy Berger: More Than You Ever Wanted to Know About Protein & Gluconeogenesis
Of all the myths and misinformation I wish we could kill, strap to a block of concrete, and push off the side of a boat in very deep, shark-infested waters, the protein = sugar thing is close to the top.0 -
AlabasterVerve wrote: »Blog post by Amy Berger: More Than You Ever Wanted to Know About Protein & Gluconeogenesis
Of all the myths and misinformation I wish we could kill, strap to a block of concrete, and push off the side of a boat in very deep, shark-infested waters, the protein = sugar thing is close to the top.
I must disagree. My conclusions are not scientific, but come from anecdotal observations from:
1. Being a type 1 diabetic, testing BG multiple times daily for decades;
2. Using a CGM fairly consistently for many years (not quite 1 decade yet);
3. Discussing the topic with others fitting 1 and sometimes 2 (above) of how protein affects BG;
4. Discussing the topic with those who do not fit either 1 or 2 above, but follow a ketogenic diet; and
5. Eating a standard American diet for most of my life;
6. Switching to moderately low carb in Mar. 2016 and gradually decreasing over several months until now, when I consume a 'zero carb' diet.
From all of my observations, I've found that some of us convert protein to glucose just because excess protein is available. Some of us do not. I haven't yet figured out what is different between those that do and those that do not.
Here is a recent personal (anecdotal) example (this happened last night, but a similar thing happened a couple days ago when I ate the same food in a large quantity):
I ate a large amount (18 oz.) of pork roast. I cooked it myself, added nothing during the cooking process nor after cooking. It was just a chunk of meat, and I will acknowledge it was not "lean" meat.
-About 2 hours later, my BG had risen to nearly 300 mg/dl.
-I took some insulin, ran for 45 min., and lifted weights.
-After the insulin and exercise, my BG had dropped to just below 200 mg/dl. I took some additional insulin to continue to bring it down and went to sleep.
-About 5 hrs. post-meal, I awoke and tested at almost 160 mg/dl. This is still high, so I took another correction dose of insulin.
-At about 12 hours after eating, I awoke this morning to a BG of 290 mg/dl.
How could my BG have risen so sharply so quickly after eating a chunk of meat? Also, how did it rise so much from 5 hrs. to 12 hrs.? It is because excess protein (and possibly some of the fat) converts to glucose... just because it is there, not because I needed it. It takes hours for all of this conversion to occur and some people will tell you they don't have this type of experience, but some of us do.0 -
"How could my BG have risen so sharply so quickly after eating a chunk of meat?"
Perhaps the diabetic portion of the blog post may be of interest to you:
If we’re talking about type 1 and type 2 diabetics, it’s a different story.
Take type 1 diabetes:
Type 1 diabetics secrete little to no insulin. That means they have no way of countering the effects of glucagon. (This is why their BG goes so high. It’s glucagon run amok, and I wrote about it here.) So if a T1 diabetic eats a lot of protein in one sitting, they will have a big blood glucose rise. In the absence of insulin, the glucagon secretion induced by protein is going to tell the liver to keep pumping out glucose, nonstop, and maybe also tell skeletal muscle to break down proteins to release amino acids that can be used as fuel or sent to the liver, to be converted into glucose. Adipose tissue (fat cells) will also hemorrhage fatty acids, because glucagon stimulates lipolysis. All around, this is bad news, and it’s why T1 diabetics waste away without insulin pretty much no matter what they eat. Protein stimulating glucagon release is, at least in part, why T1 diabetics have to bolus their insulin to match their protein intake in addition to their carbohydrate intake. (This is what spurred Marty Kendall to start creating his super-extra-awesome insulin index of foods – it was to help his wife, who has T1D, better regulate her BG.)2 -
AlabasterVerve wrote: »"How could my BG have risen so sharply so quickly after eating a chunk of meat?"
Perhaps the diabetic portion of the blog post may be of interest to you:
If we’re talking about type 1 and type 2 diabetics, it’s a different story.
Take type 1 diabetes:
Type 1 diabetics secrete little to no insulin. That means they have no way of countering the effects of glucagon. (This is why their BG goes so high. It’s glucagon run amok, and I wrote about it here.) So if a T1 diabetic eats a lot of protein in one sitting, they will have a big blood glucose rise. In the absence of insulin, the glucagon secretion induced by protein is going to tell the liver to keep pumping out glucose, nonstop, and maybe also tell skeletal muscle to break down proteins to release amino acids that can be used as fuel or sent to the liver, to be converted into glucose. Adipose tissue (fat cells) will also hemorrhage fatty acids, because glucagon stimulates lipolysis. All around, this is bad news, and it’s why T1 diabetics waste away without insulin pretty much no matter what they eat. Protein stimulating glucagon release is, at least in part, why T1 diabetics have to bolus their insulin to match their protein intake in addition to their carbohydrate intake. (This is what spurred Marty Kendall to start creating his super-extra-awesome insulin index of foods – it was to help his wife, who has T1D, better regulate her BG.)
Ugh. To say I got cheated in life sounds like a gross under-statement.
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AlabasterVerve wrote: »Blog post by Amy Berger: More Than You Ever Wanted to Know About Protein & Gluconeogenesis
Of all the myths and misinformation I wish we could kill, strap to a block of concrete, and push off the side of a boat in very deep, shark-infested waters, the protein = sugar thing is close to the top.
Amazing blog post. Thank you so much for sharing this. I have never seen GNG and post protein BG rise explained so well.
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Postprandial energy metabolism and substrate oxidation in response to the inclusion of a sugar- or non-nutritive sweetened beverage with meals differing in protein content
Conclusion
Appetite sensations, food preferences, energy expenditure and substrate oxidation are significantly altered in response to changes in meal macronutrient composition produced by modifications in the protein content of a meal and consumption of a SSB. Most notably, consumption of a SSB during a meal markedly reduces energy efficiency and fat oxidation independent of macronutrient composition.
Discussion
The primary goal of this research was to determine the extent to which the addition of a SSB to standardized meals differing in dietary protein impacts appetite, energy metabolism and substrate oxidation. We found that SSB consumption modifies meal-induced alterations in food preferences, energy expenditure and substrate oxidation, thus, impacting both sides of the energy balance equation.
On the intake side, the additional energy intake from the SSB did not influence satiety and the desire to eat savory and salty foods was increased when paired with a protein-rich meal. On the expenditure side, SSB consumption increased energy expenditure by 80 kcal, thus, creating a 40 kcal excess which was independent of dietary protein. SSB also decreased postprandial fat oxidation by 8%.
These results highlight the impact SSB consumption can have on energy balance and substrate oxidation and provides further insight into the potential role of SSBs in the etiology of obesity.
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Pretreatment fasting plasma glucose and insulin modify dietary weight loss success: results from 3 randomized clinical trials
Results:
In the DiOGenes trial, prediabetic individuals regained a mean of 5.83 kg (95% CI: 3.34, 8.32 kg; P < 0.001) more on the high– than on the low–glycemic load diet, whereas normoglycemic individuals regained a mean of 1.44 kg (95% CI: 0.48, 2.41 kg; P = 0.003) more [mean group difference: 4.39 kg (95% CI: 1.76, 7.02 kg); P = 0.001].
In SHOPUS, prediabetic individuals lost a mean of 6.04 kg (95% CI: 4.05, 8.02 kg; P < 0.001) more on the New Nordic Diet than on the control diet, whereas normoglycemic individuals lost a mean of 2.20 kg (95% CI: 1.21, 3.18 kg; P < 0.001) more [mean group difference: 3.84 kg (95% CI: 1.62, 6.06 kg); P = 0.001].
In NUGENOB, diabetic individuals lost a mean of 2.04 kg (95% CI: −0.20, 4.28 kg; P = 0.07) more on the high-fat and low-carbohydrate diet than on the low-fat and high-carbohydrate diet, whereas normoglycemic individuals lost a mean of 0.43 kg (95% CI: 0.03, 0.83 kg; P = 0.03) more on the low-fat and high-carbohydrate diet [mean group difference: 2.47 kg (95% CI: 0.20, 4.75 kg); P = 0.03]. The addition of FI strengthened these associations.
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Effects of Popular Diets without Specific Calorie Targets on Weight Loss Outcomes: Systematic Review of Findings from Clinical Trials
Literature searches were conducted through PubMed, Cochrane Library, and Web of Science using preset key terms to identify all relevant clinical trials for these 20 diets. A total of 16 articles were identified which reported findings of clinical trials for seven of these 20 diets:
(1) Atkins;
(2) Dietary Approaches to Stop Hypertension (DASH);
(3) Glycemic-Index;
(4) Mediterranean;
(5) Ornish;
(6) Paleolithic; and
(7) Zone.
Of the diets evaluated, the Atkins Diet showed the most evidence in producing clinically meaningful short-term (≤six months) and long-term (≥one-year) weight loss. Other popular diets may be equally or even more effective at producing weight loss, but this is unknown at the present time since there is a paucity of studies on these diets.
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Like petting puppies: Altered Dopamine Synaptic Markers in Postmortem Brain of Obese Subjects
Neurobiological changes in presynaptic DA markers demonstrated postmortem in human brain support a link between hedonic DA dysregulation and obesity.
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Cochrane Review: Low glycaemic index diets for the prevention of cardiovascular disease
There is currently no evidence available regarding the effect of low GI diets on cardiovascular disease events. Moreover, there is currently no convincing evidence that low GI diets have a clear beneficial effect on blood lipids or blood pressure parameters.
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Timeline of changes in appetite during weight loss with a ketogenic diet
Background/objective: Diet-induced weight loss (WL) leads to increased hunger and reduced fullness feelings, increased ghrelin and reduced satiety peptides concentration (glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK) and peptide YY (PYY)). Ketogenic diets seem to minimise or supress some of these responses. The aim of this study was to determine the timeline over which changes in appetite occur during progressive WL with a ketogenic very-low-energy diet (VLED).
Conclusions:
Weight loss with a ketogenic VLED transiently increases the drive to eat up to 3 weeks (5% WL). After that, and while participants are ketotic, a 10–17% WL is not associated with increased appetite. However, hunger feelings and active ghrelin concentrations increase significantly from baseline, once refeeding occurs.
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Evaluation of diet pattern and weight gain in postmenopausal women enrolled in the Women’s Health Initiative Observational Study
It is unclear which of four popular contemporary diet patterns is best for weight maintenance among postmenopausal women. Four dietary patterns were characterised among postmenopausal women aged 49–81 years (mean 63·6 (sd 7·4) years) from the Women’s Health Initiative Observational Study:
(1) a low-fat diet;
(2) a reduced-carbohydrate diet;
(3) a Mediterranean-style (Med) diet; and
(4) a diet consistent with the US Department of Agriculture’s Dietary Guidelines for Americans (DGA).
By baseline weight status, the reduced-carbohydrate diet was inversely related to weight gain among women who were normal weight (OR 0·72; 95 % CI 0·63, 0·81), overweight (OR 0·67; 95 % CI 0·59, 0·76) or obese class I (OR 0·63; 95 % CI 0·53, 0·76) at baseline. The low-fat diet was associated with increased risk of weight gain in women who were normal weight (OR 1·28; 95 % CI 1·13, 1·46), overweight (OR 1·60; 95 % CI 1·40, 1·83), obese class I (OR 1·73; 95 % CI 1·43, 2·09) or obese class II (OR 1·44; 95 % CI 1·08, 1·92) at baseline.
These findings suggest that a low-fat diet may promote weight gain, whereas a reduced-carbohydrate diet may decrease risk of postmenopausal weight gain.
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Conversion of Sugar to Fat: Is Hepatic de Novo Lipogenesis Leading to Metabolic Syndrome and Associated Chronic Diseases?
Epidemiologic studies suggest a link between excess sugar consumption and obesity, fatty liver disease, metabolic syndrome, and type 2 diabetes mellitus. One important pathway that may link these metabolic diseases to sugar consumption is hepatic conversion of sugar to fat, a process known as de novo lipogenesis (DNL).
Mechanistic studies have shown that diets high in simple sugars increase both DNL and liver fat. Importantly, removal of sugar from diets of children with obesity for only 9 days consistently reduced DNL and liver fat and improved glucose and lipid metabolism.
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carbohydrate-induced DNL appears to be specific to simple carbohydrates. Timlin and Parks25 demonstrated that when simple sugars are restricted and a diet high in complex carbohydrates (eg, starch) is consumed, DNL is trivial after an overnight fast.
Likewise, in the fed state, DNL is also determined by the type of simple sugar consumed. Fructose, but not glucose, increased hepatic DNL in 6 healthy lean participants (Figure 3).9 During 6 hours of fructose ingestion, DNL increased 20-fold, and 25% of circulating VLDL-TG was derived from DNL.
In contrast, when the study was repeated in the same participants using glucose levels, rates of DNL were unaffected, and only 1% to 2% of VLDL-TG was synthesized de novo. These data demonstrate that fructose is a potent stimulus to lipogenesis.
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There is evidence that both hyperinsulinemia and a diet rich in simple sugars, by promoting DNL, contribute to hypertriglyceridemia and liver fat accumulation and, ultimately, to metabolic syndrome.30
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studies demonstrated that in patients with insulin-resistance, fasting DNL is increased even under circumstances in which carbohydrate intake is limited, suggesting that hyperinsulinemia per se stimulates DNL.
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Hepatic glucose production, which is typically suppressed by high insulin levels, was not blunted by a high-fructose diet. This hepatic insulin resistance may contribute to the development of type 2 diabetes.
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Conclusion
Chronically elevated DNL during both fasting and feeding may be a key mechanism in the link between consumption of added sugar and metabolic abnormalities, including obesity, high lipid levels, cardiovascular disease, NAFLD, insulin resistance, and type 2 diabetes.
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Clinical Outcomes of Dietary Replacement of Saturated Fatty Acids with Unsaturated Fat Sources in Adults with Overweight and Obesity: A Systematic Review and Meta-Analysis of Randomized Control Trials
Conclusions: Due to null results and a small number of studies included, there is no strong evidence that replacement of SFA with UFA may benefit lipid profiles in this population.
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Eat more meat.
Headline: Historic Discovery Promises to Prevent Miscarriages and Birth Defects Globally- One of the greatest discoveries in pregnancy research
- Vitamin B3 can cure molecular deficiencies which cause miscarriages and birth defects
- Discovery promises to significantly reduce miscarriages and birth defects
- Findings expected to change the way pregnant women are cared for
"a recent study found that despite taking vitamin supplements at least a third of pregnant women have low levels of vitamin B3 in their first trimester, which is the critical time in organ development. By the third trimester, vitamin B3 levels were low in 60% of pregnant women. This indicates pregnant women may require more vitamin B3 than is currently available in most vitamin supplements."
Update: Under no circumstances do we want to offer false hope to families who have been affected by miscarriage or birth defects. However, our research provides strong evidence that vitamin B3 has the potential to prevent these terrible outcomes in some cases. The Victor Chang Institute would never suggest that this discovery will explain all causes of miscarriage and birth defects.
It is not known how many cases of miscarriage and birth defects are caused by low levels of NAD. It is also not yet known what dose of vitamin B3 will prevent miscarriage and birth defects. Further research in this important area is underway at the Victor Chang Institute.
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Repeat. I posted this earlier.0
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I imagine a lot of people on MFP would like this article:
The Best Fat Loss Article on the Motherfuckin’ Internet
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AlabasterVerve wrote: »I imagine a lot of people on MFP would like this article:
The Best Fat Loss Article on the Motherfuckin’ Internet
This was a really great article if you've got the time to read the whole thing. Also funny, which I totally appreciate.1 -
Dynamics of intrapericardial and extrapericardial fat tissues during long-term, dietary-induced, moderate weight loss
Results: The 18-mo moderate weight loss was similar in both groups, but the reduction in waist circumference was higher in the Mediterranean/low-carbohydrate group than in the low-fat diet group. After 18 mo, the intrapericardial-fat volume had reduced twice as much in the MED/LC group compared with the LF group.
Note: The carb restriction between the two groups was modest, about 10%. (Ludwig)
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Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study
Interpretation
High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.
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Fruit, vegetable, and legume intake, and cardiovascular disease and deaths in 18 countries (PURE): a prospective cohort study
Interpretation
Higher fruit, vegetable, and legume consumption was associated with a lower risk of non-cardiovascular, and total mortality. Benefits appear to be maximum for both non-cardiovascular mortality and total mortality at three to four servings per day (equivalent to 375–500 g/day).
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PURE study links
Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from
five continents (PURE): a prospective cohort study: link
Fruit, vegetable, and legume intake, and cardiovascular disease and deaths in 18 countries (PURE): a prospective
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Possible explanation why some find it easier to not to eat at all than to stop eating once they start?
Feeding releases endogenous opioids in humans
Eating both bland (left panel) and delicious (right panel) meals triggered significant opioid release in the brain.
The opioid system regulates eating and appetite, and we have previously found that its dysfunctions are a hallmark of morbid obesity. The present results suggest that overeating may continuously overstimulate the opioid system, thus directly contributing to development of obesity.
Media
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Efficacy of low carbohydrate diet for type 2 diabetes mellitus management: A systematic review and meta-analysis of randomized controlled trials.
CONCLUSIONS:
The results suggested a beneficial effect of LCD intervention on glucose control in patients with type 2 diabetes. The LCD intervention also had a positive effect on triglycerides and HDL cholesterol concentrations, but without significant effect on long term weight loss.
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