More Science, Can You Believe It?

Oh yes that's an excellent one, here

http://sci-hub.tw/10.1002/jcla.22650

There's just so much of it now

Relationship between very low low-density
lipoprotein cholesterol concentrations not
due to statin therapy and risk of type 2
diabetes: A US-based cross-sectional
observational study using electronic health
records

https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002642

"Very low LDL-C concentrations occurring in the absence of statin treatment were significantly associated with T2DM risk in a large EHR population; this increased risk was present in both sexes and all BMI categories, and in individuals of European ancestry but not of African ancestry. Longitudinal cohort studies to assess the relationship between very low LDL-C levels not associated with lipid-lowering therapy and risk of developing T2DM will be important."

oops!

Remission of pre-diabetes to normal
glucose tolerance in obese adults with
high protein versus high carbohydrate
diet: randomized control trial

https://drc.bmj.com/content/4/1/e000258

Still a bit afraid of the fat, but even cutting carbs to 40% seems to help

Comparison of endothelial progenitor cell
function in type 2 diabetes with good and poor
glycemic control

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858721/

"Conclusion

There was EPC dysfunction in type 2 diabetes which might be improved by strict glycemic control. However, the circulating EPC number and proliferative function in patients with good glycemic control did not reach the level in healthy controls."

I suspect that may be due to the way control was achieved. Low carb good, jacking up insulin bad. Just a thought. Ties in with much of Malcolm Kendrick's work.

This study was done eight years ago and don't think there have been any other studies that contradict it

Markers of cardiovascular risk are not changed by increased whole-grain intake: the WHOLEheart study, a randomised, controlled dietary intervention

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3501710/

More recently and one which dietitians must hate 

Whole grain cereals for the primary or secondary prevention of cardiovascular disease.

https://www.ncbi.nlm.nih.gov/pubmed/28836672

That first one contained Susan Jebb. oops!

Yes the Cochrane one didn't go down so well.

Where are the studies of whole grains vs. NO grains?

https://isupportgary.com/articles/seventh-day-adventist-plant-based-nutrition

https://isupportgary.com/articles/cereal-catalyst-lifestyle-medicine-vegan

Role Of Sugars in Human Neutrophilic Phagocytosis - from 1973

http://sci-hub.tw/10.1093/ajcn/26.11.1180

Risk Factors, Mortality, and Cardiovascular
Outcomes in Patients with Type 2 Diabetes

http://sci-hub.tw/10.1056/NEJMoa1800256

Association between insulin resistance
and the development of cardiovascular disease

https://cardiab.biomedcentral.com/articles/10.1186/s12933-018-0762-4

pdf available

The Food Supply Of The Future (from 1909)

https://www.jstor.org/stable/pdf/1634378.pdf

Output and technical change in twentieth-century
British agriculture

http://www.bahs.org.uk/AGHR/ARTICLES/48n1a4.pdf

long but interesting

and another excellent takedown of Harvard/Lancet rubbish

https://www.psychologytoday.com/us/blog/diagnosis-diet/201809/latest-low-carb-study-all-politics-no-science

ASSOCIATIONS BETWEEN TRIGLYCERIDE/HIGH-DENSITY LIPOPROTEIN CHOLESTEROL RATIO AND MICRO- AND MACROANGIOPATHIES IN TYPE 2 DIABETES MELLITUS

Conclusion: A high TG/HDL-C ratio was significantly associated with albuminuria, CAD, CVA, and peripheral artery occlusive disease (PAOD) in patients with DM, which translated into an increased risk of cardiovascular disease.

http://journals.aace.com/doi/abs/10.4158/EP-2017-0254?code=aace-site&journalCode=endp

Another earlier study stressing the importance TG/HDL ratio

The Association between Triglyceride/High-Density Lipoprotein Cholesterol Ratio and All-Cause Mortality in Acute Coronary Syndrome after Coronary Revascularization

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0123521

Of course we know how to lower trigs and raise HDL don't we 

Meanwhile found on twitter via Ivor, new from Uffe Ravnskov

LDL-C Does Not Cause Cardiovascular Disease: a comprehensive review of current literature

Expert commentary

Our search for falsifications of the cholesterol hypothesis confirms that it is unable to satisfy any of the Bradford Hill criteria for causality, and that the conclusions of the authors of the three reviews are based on misleading statistics, exclusion of unsuccessful trials and by ignoring numerous contradictory observations.

https://www.tandfonline.com/doi/abs/10.1080/17512433.2018.1519391

Damn, the first paper isn't on Sci-Hub (yet) but the Ravnskov one is

https://doi.org/10.1080/17512433.2018.1519391

It's getting to the state where the only people who don't know this stuff have their fingers in their ears.

Meanwhile Jennifer Elliott is back blogging again

http://blog.babyboomersandbellies.com

and here's one of her papers

Flaws, Fallacies and Facts: Reviewing the
Early History of the Lipid and Diet/Heart
Hypotheses

http://file.scirp.org/Html/7-2701370_50455.htm

no wonder they had to deregister her

Just from the abstract of the Uffe Ravnskov paper it's plain to see were he's coming from, wonder if Professor Statin has read it yet 

Another paper from Nicola Guess, she seems to be one of the saner ones who's prepared to consider diets other than low fat 

Dietary Interventions for the Prevention of Type 2 Diabetes in High-Risk Groups: Current State of Evidence and Future Research Needs

Abstract: A series of large-scale randomised controlled trials have demonstrated the effectiveness of lifestyle change in preventing type 2 diabetes in people with impaired glucose tolerance. Participants in these trials consumed a low-fat diet, lost a moderate amount of weight and/or increased their physical activity. Weight loss appears to be the primary driver of type 2 diabetes risk reduction, with individual dietary components playing a minor role. The effect of weight loss via other dietary approaches, such as low-carbohydrate diets, a Mediterranean dietary pattern, intermittent fasting or very-low-energy diets, on the incidence of type 2 diabetes has not been tested. These diets—as described here—could be equally, if not more effective in preventing type 2 diabetes than the tested low-fat diet, and if so, would increase choice for patients. There is also a need to understand the effect of foods and diets on beta-cell function, as the available evidence suggests moderate weight loss, as achieved in the diabetes prevention trials, improves insulin sensitivity but not beta-cell function. Finally, prediabetes is an umbrella term for different prediabetic states, each with distinct underlying pathophysiology. The limited data available question whether moderate weight loss is effective at preventing type 2 diabetes in each of the prediabetes subtypes.

http://www.mdpi.com/2072-6643/10/9/1245/htm

Obviously a moderate weight loss would not have prevented my diabetes 

Nor mine, nor that of about 20% of other "Type 2"s.

I can't decide about her, she's less clueless than the other reprobates but still has a long way to go. A while back she was stating that there was "no evidence" other than made up stuff on blogs about the harms from Omega 6 oils, and Tucker Goodrich kindly pointed her to not just a paper but an entire ISSUE of a journal on the subject. It's hard to do evidence-based medicine when you aren't told about half the evidence.

Still she's moving in the right direction. I think the next step will be

"Well if you really can't make a healthy low fat/Mediterranean?vegan diet work perhaps it wouldn't do any harm to try a low carb diet, but only for six months"

To us it's woeful but to them it's a major step.

Not read the full  paper yet but it's promising research into cancer

Mitochondrial Correction: A New Therapeutic Paradigm for Cancer and Degenerative Diseases

https://www.isom.ca/article/mitochondrial-correction-new-therapeutic-paradigm-cancer-degenerative-diseases/

High fat vindicated in this new study

Mechanisms Preserving Insulin Action during High Dietary Fat Intake

Highlights

• Insulin sensitivity is maintained in both men and mice with high PUFA or SFA intake
  
• Hepatic glucose production and de novo lipogenesis are decreased with high fat intake
  
• High fat intake decreases fasting insulin and triacylglycerol levels
  
• High fat intake changes the plasma proteome in an immune-supporting direction
  

https://www.cell.com/cell-metabolism/fulltext/S1550-4131(18)30565-5

http://sci-hub.tw/10.1016/j.cmet.2018.08.022

meanwhile

Extra-intestinal manifestations of non-celiac gluten
sensitivity: an expanding paradigm

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5897856/

ties in nicely with the recent one about gluten in the diet of mothers and subsequent Type 1 diabetes in their children

Gives the lie to this somewhat

https://www.nutritioncoalition.us/news/2018/9/10/big-pasta-cooks-up-self-interested-nutrition-science

Omega-6 vegetable oils as a driver of
coronary heart disease: the oxidized
linoleic acid hypothesis

https://openheart.bmj.com/content/openhrt/5/2/e000898.full.pdf

not so heart healthy after all huh?

Mechanisms Preserving Insulin Action during High
Dietary Fat Intake

http://sci-hub.tw/10.1016/j.cmet.2018.08.022

a technical look at the changes that occur without the customary paranoia

Effect of Chronic Hyperglycemia on Glucose Metabolism in Subjects with Normal Glucose
Tolerance

http://sci-hub.tw/10.2337/db18-0439

likewise

Dietitians won't like this

Effects of Various Commercial Whole-Grain Breads on Postprandial Blood Glucose Response and Glycemic Index in Healthy Subjects 

Postprandial hyperglycemia is a serious risk factor for cardiovascular disease and type 2 diabetes mellitus (T2DM). As diet is a cornerstone of both T2DM prevention and therapy, we investigated the effects of various commercially available breads on postprandial glucose response and glycemic index. Furthermore, the impact of oilseed- and protein-enriched breads was evaluated, as well as the influence of different wheat flour coarseness settings. Three experiments were conducted to study the effects of various breads on the postprandial glucose levels of randomly selected subjects (42 in total). First, putative differences of seven types of commercially available whole-grain breads were studied. Second, the influence of oilseed- and protein-enriched breads was investigated and third, the influence of different wheat flour coarseness settings was characterized. The total area under curve (AUC), postprandial glucose response, peak glucose level and glycemic index were calculated for each condition. Consumption of various types of whole-grain breads resulted in large variations in postprandial glucose response and significant differences in calculated glycemic indices. Furthermore, postprandial glucose levels and glycemic indices appeared significantly lower for protein-rich bread than compared to oil-seed-rich bread. Interestingly, no significant differences in postprandial glucose levels or glycemic indices were detected for fine, medium or coarse wheat flour breads. Based on the correlation study, breads with low total carbohydrates and high amounts of protein are advisable for the prevention of high glucose loads and should be considered by people suffering from T2DM. Trial registration: O2413 (Ethics Commissions of Upper Austria) 

https://www.researchgate.net/publication/324746855_Effects_of_Various_Commercial_Whole-Grain_Breads_on_Postprandial_Blood_Glucose_Response_and_Glycemic_Index_in_Healthy_Subjects

PDF available

Not sure if I've posted this before or not 

HbA1c variability is a powerful, independent measure, regardless of how it is measured

http://www.physiciansbriefing.com/Article.asp?AID=737869

My A1c has remained stable over the past ten years just another benefit of low carb 

But . . . but . . . but . . . GRAINZ!!!

Backs up the recent research by Michael Snyder using a CGM. Cornflakes for breakfast were driving diabetic numbers in many nondiabetics. Did I post that one up the thread or have I to find it again?

I think it was this one

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6057684/

The second one is here

http://sci-hub.tw/10.1111/dom.13306

My A1c has varied a bit but stayed below 6% for 14 years now. That's the way to do it! Well nearly, some (including Type 1s) get below 5%

My favourite (classic) papers on the subject

EPIC Norfolk

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC26599/pdf/15.pdf

Elley et al

http://sci-hub.tw/10.1111/j.1464-5491.2008.02581.x

Brewer et al

http://care.diabetesjournals.org/content/diacare/31/6/1144.full.pdf

all looking at the correlation of A1c and cardiovascular risk or premature death

There's one I can't recall just now (actually I think more than one) that correlates A1c with microvascular complications and postprandial glucose spikes with macrovascular complications.

Then there's this

Twelve-month outcomes of a randomized
trial of a moderate-carbohydrate versus
very low-carbohydrate diet in overweight
adults with type 2 diabetes mellitus or
prediabetes

https://www.nature.com/articles/s41387-017-0006-9.pdf

and from ten years ago

The effect of a low-carbohydrate, ketogenic diet versus a
low-glycemic index diet on glycemic control in type 2 diabetes
mellitus

https://nutritionandmetabolism.biomedcentral.com/track/pdf/10.1186/1743-7075-5-36

Yet dieticians still bleat that there is no evidence. Well of course there isn't when you don't look at it.

Hyperinsulinemia: a Cause of Obesity?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5487935/pdf/13679_2017_Article_261.pdf

Barbara Corkey is a credible researcher. So is Jim Johnson, who now works for Novo Nordisk in Oxford, and Gareth Lim who now has his own lab

https://www.researchgate.net/publication/312080213_A_causal_role_for_hyperinsulinemia_in_obesity

Oh and another post from Joy Kiddie

http://www.lchf-rd.com/2018/09/28/a-trial-of-the-evidence/

looks like Australia is moving fast in the right direction.

Effects of intensive interventions compared to standard care in people with type 2 diabetes and microalbuminuria on risk factors control and cardiovascular outcomes: a systematic review and meta-analysis of randomised controlled trials

Conclusions
Apart from blood pressure outcomes, there was no evidence that intensive interventions improve or worsen HbA1c, total cholesterol, LDL, triglycerides, urinary albumin excretion rate, risk of cardiovascular or mortality outcomes in people with type 2 diabetes and microalbuminuria. Results of this review are mainly influenced by one small trial, hence uncertainty surrounding the effect of intensive interventions in people with type 2 diabetes and microalbuminuria still exists. Large studies are urgently required in this high risk cardiovascular group of patients.

https://www.diabetesresearchclinicalpractice.com/article/S0168-8227(18)31245-2/fulltext

Given some of the controversy from recent epidemiological studies this puts things into perspective

Controversy and debate: memory-based methods paper 1: the fatal flaws of food frequency questionnaires and other memory-based dietary assessment methods


Abstract
There is an escalating debate over the value and validity of self-reported dietary intake as estimated by Food Frequency Questionnaires and other forms of memory-based dietary assessment methods. Proponents argue that despite limitations, memory-based methods provide valid and valuable information about consumed foods and beverages and therefore can be used to assess diet-disease relations. In fact, over the past 60 years, thousands of memory-based dietary research reports were used to inform public policy and establish the Dietary Guidelines for Americans. Yet, despite this impressive history, our position is that memory-based dietary assessment methods are invalid and inadmissible for scientific research and therefore cannot be used in evidence-based policy making. Herein, we present the empirical evidence and theoretic and philosophic perspectives that render data derived from memory-based methods both fatally flawed and pseudoscientific. First, the use of memory-based methods is founded upon two inter-related logical fallacies: a category error and reification. Second, human memory and recall are not valid instruments for scientific data collection. Third, in standard epidemiologic contexts, the measurement errors associated with self-reported data are nonfalsifiable because there is no way to ascertain if the reported foods and beverages match the respondent’s actual consumption. Fourth, the assignment of nutrient and energy values to self-reported intake (i.e., the pseudoquantification of anecdotal data) is impermissible and violates the foundational tenets of measurement theory. Fifth, the proxy estimates created via pseudoquantification are often physiologically implausible and have little relation to actual nutrient and energy consumption.Finally, investigators engendered a fictional discourse on the health effects of dietary sugar, salt, fat and cholesterol when they failed to cite contrary evidence or address decades of research demonstrating the fatal measurement, analytic, and inferential flaws of memory-baseddietary assessment methods.

https://www.jclinepi.com/article/S0895-4356(17)31375-6/pdf

Oh yes that was excellent!

The first one

http://sci-hub.tw/10.1016/j.diabres.2018.10.002

Shows the problem with replacing high glucose with high insulin and finding neither are good for you.

Meanwhile

https://www.nutritionadvance.com/health-benefits-saturated-fat/

one of the quoted papers here

http://sci-hub.tw/10.1001/jamainternmed.2016.5394

Must take from this that noxious dietitians are part of the problem 

Carbotoxicity—Noxious Effects of Carbohydrates

Modern nutrition is often characterized by the excessive intake of different types of carbohydrates ranging from digestible polysaccharides to refined sugars that collectively mediate noxious effects on human health, a phenomenon that we refer to as “carbotoxicity.” Epidemiological and experimental evidence combined with clinical intervention trials underscore the negative impact of excessive carbohydrate uptake, as well as the beneficial effects of reducing carbs in the diet. We discuss the molecular, cellular, and neuroendocrine mechanisms that link exaggerated carbohydrate intake to disease and accelerated aging as we outline dietary and pharmacologic strategies to combat carbotoxicity.

https://www.cell.com/cell/fulltext/S0092-8674(18)30972-3

Oscillating Glucose Is More Deleterious to Endothelial
Function and Oxidative Stress Than Mean Glucose in
Normal and Type 2 Diabetic Patients

http://diabetes.diabetesjournals.org/content/57/5/1349

CONCLUSIONS—These data suggest that oscillating glucose
can have more deleterious effects than constant high glucose on
endothelial function and oxidative stress, two key players in
favoring cardiovascular complications in diabetes. Concomitant
vitamin C infusion can reverse this impairment

some of the references may be worth a look, I recall studies where microvascular complications tracked with A1c and macrovascular complications tracked with postprandial glucose spikes - and when the spikes are brief enough the blood is only glycated reversibly, while other tissues don't have that luxury

Paradox of hypercholesterolaemia in highly trained, keto-adapted athletes

https://bmjopensem.bmj.com/content/4/1/e000429

Volek Phinney et al look into the background of what Dave Feldman has been researching

A Reappraisal of the Lipid Hypothesis

https://www.amjmed.com/article/S0002-9343(18)30404-2/pdf

"UNINTENDED CONSEQUENCES
Promoting foods that are low in cholesterol but typically
high in refined carbohydrates is supposed to help prevent
coronary heart disease. Paradoxically, there is now evidence
that these dietary changes have contributed to the
epidemic of diabetes that can actually lead to coronary
heart disease.20 Furthermore, some statin users mistakenly
believe they can eat whatever they want, leading to the phenomenon
of statin gluttony.21 Consider also that the recent
expansion of statin indications may result in millions of
healthy individuals being treated because of a risk score
even though they may be at extremely low risk of coronary
heart disease."

The insulin resistance syndrome: impact on lipoprotein
metabolism and atherothrombosis
Henry N. Ginsberg and Li-Shin Huang

http://sci-hub.tw/http://doi.org/10.1177/204748730000700505

Insulin Resistance as a Predictor of
Age-Related Diseases

https://academic.oup.com/jcem/article/86/8/3574/2848584

both these are from EIGHTEEN years ago, the second starring Gerald Reaven

graham64 wrote:Must take from this that noxious dietitians are part of the problem 

Carbotoxicity—Noxious Effects of Carbohydrates

Modern nutrition is often characterized by the excessive intake of different types of carbohydrates ranging from digestible polysaccharides to refined sugars that collectively mediate noxious effects on human health, a phenomenon that we refer to as “carbotoxicity.” Epidemiological and experimental evidence combined with clinical intervention trials underscore the negative impact of excessive carbohydrate uptake, as well as the beneficial effects of reducing carbs in the diet. We discuss the molecular, cellular, and neuroendocrine mechanisms that link exaggerated carbohydrate intake to disease and accelerated aging as we outline dietary and pharmacologic strategies to combat carbotoxicity.

https://www.cell.com/cell/fulltext/S0092-8674(18)30972-3

http://sci-hub.tw/10.1016/j.cell.2018.07.044

looks excellent, I'll read it later

Oh yes that WAS excellent.

Novel subgroups of adult-onset diabetes and their association
with outcomes: a data-driven cluster analysis of six variables

http://sci-hub.tw/10.1016/S2213-8587(18)30051-2

moving in the right direction but not quite there yet, looking at the different subtypes of "diabetes"

Roger Unger is king of the alpha cells and glucagon, here's more research on the subject

http://sci-hub.tw/10.1038/s41574-018-0097-y

Interesting article as always from the estimable Jim Johnson

https://www.endocrinology.org/endocrinologist/129-autumn18/features/endogenous-insulin-its-role-in-the-initiation-progression-and-management-of-diabetes/

This headline caught my eye, another paper casting doubt on the diet-heart hypothesis 

OF COWS AND MEN: REVIEWING THE LINK BETWEEN MILK FAT AND HUMAN HEALTH 

CONCLUSION
We may be in the midst of a paradigm shift in human nutrition. The revaluation of the validity of classic literature and the emerging plethora of evidence over the past decade, strongly contradict the long-held idea that dietary saturated fats cause adverse effects on health. Moreover, as shown in this review, current evidence indicates that dairy products,
including full-fat dairy, may exert protective effects on metabolic health, reducing the incidence of obesity, T2D, MetS, CVD, and mortality. In light of this evidence, a general call to revise the guidelines on dairy consumption seems strongly justified and necessary, particularly as dairy products may help combat the spread of chronic diseases. Moreover, the historic focus on individual nutrients (e.g., fat, calories) has proven limited in terms of predicting clinical outcomes. In this sense, a whole-food approach to studying the effects of the ensemble of nutrients contained in dairy foods on human health outcomes seems
warranted. Lastly, policy changes should be guided by a more nuanced interpretation of observational studies, and reflect the value of repeatable, randomized controlled studies, as the latter may provide insights on causality and the role of dairy on public health. 

[url=https://ecommons.cornell.edu/bitstream/handle/1813/59846/Rico (manu).pdf?sequence=2[/url]]https://ecommons.cornell.edu/bitstream/handle/1813/59846/Rico%20(manu).pdf?sequence=2[/url][/url]