THE LOW CARB DIABETIC

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THE LOW CARB DIABETIC

Promoting a low carb high fat lifestyle for the safe control of diabetes. Eat whole fresh food, more drugs are not the answer.


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    More Science, Can You Believe It?

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    Post by Long birder Sat Jul 07 2018, 14:12

    chris c wrote:The second one

    http://sci-hub.tw/10.1007/s11892-018-1017-1

    (to find full paywalled papers copy the DOI number into Sci-Hub and they will usually appear)

    I reckon I must be keeping my Vitamin D well up in the recent weather, and nitric oxide too, I spent some hours today sitting in the sun at the Hen Reedbeds not seeing many birds but chatting with some interesting people one of whom I'd met before. I've not been doing enough walking but I know the location of every seat and suitable grassy bank for miles . . .

    Yes "we know Healthy Whole Grains must be good for you despite this study not proving it". Strangely I've eaten very few of them for the last thirteen years and I strongly suspect that if I had I wouldn't still be here. They get in the way of eating Real Food.

    The fat paper was interesting, George Henderson made the point that perhaps they ate the butter on bread but the other oils in meals.

    David Ludwig and Cara Ebbeling look at the carbohydrate-insulin theory

    http://sci-hub.tw/10.1001/jamainternmed.2018.2933

    and are rapidly shot down in flames by the Usual Suspects (well that's what they think)

    http://sci-hub.tw/10.1001/jamainternmed.2018.2920


    You should read this, she really hates them.

    http://itsthewooo.blogspot.com/2018/07/the-strawman-cih-is-not-supported-by.html

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    Post by Long birder Sat Jul 07 2018, 14:19

    Can't get the full article Graham do
    you know if it's available, elsewhere?
    Derek

    graham64 wrote:Vitamin D and insulin resistance 

    https://www.jstage.jst.go.jp/article/jnsv/64/3/64_173/_pdf

    Diabetes Among Non-Overweight Individuals: an Emerging Public Health Challenge

    https://link.springer.com/article/10.1007%2Fs11892-018-1017-1
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    Post by graham64 Sat Jul 07 2018, 22:17

    Long birder wrote:Can't get the full article Graham do
    you know if it's available, elsewhere?
    Derek

    graham64 wrote:Vitamin D and insulin resistance 

    https://www.jstage.jst.go.jp/article/jnsv/64/3/64_173/_pdf

    Diabetes Among Non-Overweight Individuals: an Emerging Public Health Challenge

    https://link.springer.com/article/10.1007%2Fs11892-018-1017-1

    Hi Derek, Chris provided the link to the full text on his post check it out below  Smile

    http://sci-hub.tw/10.1007/s11892-018-1017-1
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    Post by Long birder Sun Jul 08 2018, 07:33

    graham64 wrote:
    Long birder wrote:Can't get the full article Graham do
    you know if it's available, elsewhere?
    Derek

    graham64 wrote:Vitamin D and insulin resistance 

    https://www.jstage.jst.go.jp/article/jnsv/64/3/64_173/_pdf

    Diabetes Among Non-Overweight Individuals: an Emerging Public Health Challenge

    https://link.springer.com/article/10.1007%2Fs11892-018-1017-1

    Hi Derek, Chris provided the link to the full text on his post check it out below  Smile

    http://sci-hub.tw/10.1007/s11892-018-1017-1
    Thanks Chris and Graham you guys are great sources.
    Derek
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    Post by Long birder Sun Jul 08 2018, 08:01

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    Post by chris c Sun Jul 08 2018, 21:20

    Gotta love the Wooo's rants, but first I shall need to eat something. I already had sausages and broccoli, I think a salmon (tinned) and vegetable stir fry, plus extra coffee.

    Thinking back to the Whole grains" paper, the logic is like "Rothmans are better than Woodbines so everyone must smoke more Rothmans". Very little research into "whole" grains vs. no grains.
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    Post by chris c Tue Jul 10 2018, 22:33

    Well that was fun!

    A bit of Guyenet history, once Whole Health Source was well worth a read even if you didn't necessarily agree with him, and he had a fine flock of commenters.

    Then he became a Professional Researcher. It appears he was being used to discover how to make more addictive "food" for industry although he didn't see it like that, what with his "food reward" that no-one seemed to understand. He subsequently deleted a load of his old posts, and the replies. Someone with integrity might have left them up and explained his reasoning as to why he changed his mind.

    Gary Taubes had a pop at him at a conference so he became determined to "prove" that insulin had nothing to do with obesity. In fact he tried to "prove" that insulin made you thin. I wrote on Michael Eades blog that I was going to email him and thank him for explaining how all insulin deficient Type 1s were really fat and all insulin resistant Type 2s were very slim, but he probably wouldn't notice the sarcasm.

    He ended up with a load of commenters like Carbsane, banned Woo not a few times and then had a paranoid attack that someone "in a Woo-fueled rage" was going to hunt him down and kill him.

    He's a bit more sane since then but still hates Taubes, and of course Hall was the one who caused NUSI to implode.

    Meanwhile, a near miss from Harvard

    Influence of Lifestyle on
    Incident Cardiovascular Disease and
    Mortality in Patients With
    Diabetes Mellitus

    http://sci-hub.tw/10.1016/j.jacc.2018.04.027

    would have worked better if they had a better definition of "healthy diet" and no I don't mean Willett's 63 portions of fruit and veg per day

    HbA1c, diabetes and cognitive decline: the English Longitudinal
    Study of Ageing

    https://link.springer.com/article/10.1007/s00125-017-4541-7

    pdf available. Interesting how it is those Chinese again, this time using UK data

    Metabolic flexibility as an adaptation to energy resources and
    requirements in health and disease

    http://sci-hub.tw/10.1210/er.2017-00211

    54 pages so I'm only part way through, but IMO this is what high carb diets destroy, when you are in carb overload you become incapable of metabolising fat, so when you get hungry you have to eat more carbs. Whereas the likes of us can switch seamlessly to metabolising fat, whether dietary or stored
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    Post by chris c Mon Jul 23 2018, 22:03

    Useful paper from Brazil on prediabetes - which as David Ludwig pointed out isn't really pre-anything

    http://www.scielo.br/pdf/aabc/2017nahead/0001-3765-aabc-201720160394.pdf

    "A proposal for early detection of subclinical diabetes from routine evaluation of fasting plasma insulin, which is affordable and robust and thus applicable for the general population, is further suggested."

    Couldn't agree more.
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    Post by chris c Tue Jul 31 2018, 23:52

    Cardiovascular event risk in relation to dietary fat intake in
    middle-aged individuals: data from The Malmo¨ Diet and
    Cancer Study

    http://sci-hub.tw/https://doi.org/10.1097/HJR.0b013e3282a56c45

    "Conclusions In relation to risks of cardiovascular events, our results do not suggest any benefit from a limited total or saturated fat intake, nor from relatively high intake of unsaturated fat."

    Again . . . one day even the vegans will have to notice.

    Relative contributions of preprandial and
    postprandial glucose exposures, glycemic
    variability, and non-glycemic factors to
    HbA1c in individuals with and without
    diabetes

    https://www.nature.com/articles/s41387-018-0047-8

    pdf available

    Finally science catches up with what people have been doing for decades - monitoring postprandials and controlling them through carb reduction.

    Hopefully CGMs will make this sort of thing easier to study than fingersticks.

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    Post by graham64 Wed Aug 01 2018, 21:43

    chris c wrote:Finally science catches up with what people have been doing for decades - monitoring postprandials and controlling them through carb reduction.

    Hopefully CGMs will make this sort of thing easier to study than fingersticks.

    Sadly many T2's don't even get the option of SMBG  Sad it's false economy given the right education on how to interpret the results of monitoring BG could save the NHS money on costly drugs

    There was a survey of DUK members on SMBG a few years ago

    Conclusion
    SMBG was clearly of benefit to this group of confirmed users, who used the results to adjust diet, physical activity or medications. However many individuals (particularly women) reported feelings of anxiety and depression associated with its use.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998520/
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    Post by chris c Thu Aug 02 2018, 21:51

    The classic study was by Andrew Farmer

    https://www.bmj.com/content/335/7611/132.abstract

    pdf available, and the responses are worth a read.

    "blood glucose self monitoring with additional training of patients in interpretation and application of the results to enhance motivation and maintain adherence to a healthy lifestyle "

    so they were not trained to use the results to change anything and thus failure was inevitable.

    The conventional wisdom seems to be "if we spend money on test strips now, how will we afford the amputations and dialysis?"

    Meanwhile the other classic study was by Andy Karter

    http://care.diabetesjournals.org/content/29/8/1757.full

    he actually showed that Kaiser Permanente would save money, but not many people heard of that one.

    I no longer look in the forums, has there been any change in attitude towards monitoring by doctors, other than the obvious few?
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    Post by yoly Fri Aug 03 2018, 10:35

    If doctors will at least give the correct information to the patient concerning diet and importance of watching out for glucose spikes. If the patient doesn't want to comply that will be there problem. But they don't even do that.

    On a side note. I have stopped using the glimepiride and with the diet post hurricane without processed food I been able to control with LCHF diet alone. Maybe the glimepiride kicked my pancreas into action and it may not last. But it have been a few weeks since I stopped and my glucose levels are back to normal=(non-diabetic).
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    Post by graham64 Fri Aug 03 2018, 22:32

    chris c wrote:I no longer look in the forums, has there been any change in attitude towards monitoring by doctors, other than the obvious few?

    I only go on forums occasionally these days but I've  not noticed much difference when I do have a look lots are still self funding test strips 

    Another reason not just to rely on A1c and monitor BG

    Postprandial Blood Glucose Outweighs Fasting Blood Glucose and HbA1c in screening Coronary Heart Disease

    https://www.nature.com/articles/s41598-017-14152-y
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    Post by Long birder Sat Aug 04 2018, 11:59

    graham64 wrote:
    chris c wrote:I no longer look in the forums, has there been any change in attitude towards monitoring by doctors, other than the obvious few?

    I only go on forums occasionally these days but I've  not noticed much difference when I do have a look lots are still self funding test strips 

    Another reason not just to rely on A1c and monitor BG

    Postprandial Blood Glucose Outweighs Fasting Blood Glucose and HbA1c in screening Coronary Heart Disease

    https://www.nature.com/articles/s41598-017-14152-y

    Interesting Graham for those of us who suspect we have low insulin diabetes and it is not caused directly by insulin resistance. I suspect some reactive hypoglycemics may fall into that category?
    Another reason why we should all know our insulin profiles, but money is short and I can't see that happening.
    Interesting that this population can effectively take hyperinsulinemia out of the equation with CVD as the main cause! Do you read it like that?
    regards
    Derek
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    Post by graham64 Sun Aug 05 2018, 22:21

    Long birder wrote:
    graham64 wrote:
    chris c wrote:I no longer look in the forums, has there been any change in attitude towards monitoring by doctors, other than the obvious few?

    I only go on forums occasionally these days but I've  not noticed much difference when I do have a look lots are still self funding test strips 

    Another reason not just to rely on A1c and monitor BG

    Postprandial Blood Glucose Outweighs Fasting Blood Glucose and HbA1c in screening Coronary Heart Disease

    https://www.nature.com/articles/s41598-017-14152-y

    Interesting Graham for those of us who suspect we have low insulin diabetes and it is not caused directly by insulin resistance.  I suspect some reactive hypoglycemics may fall into that category?
    Another reason why we should all know our insulin profiles, but money is short and I can't see that happening.
    Interesting that this population can effectively take hyperinsulinemia out of the equation with CVD as the main cause! Do you read it like that?
    regards
    Derek

    It certainly appears to read that way Derek they do say In conclusion, "the severity of CHD was associated with glucose rather than insulin resistance"
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    Post by chris c Mon Aug 06 2018, 23:26

    yoly wrote:If doctors will at least give the correct information to the patient concerning diet and importance of watching out for glucose spikes. If the patient doesn't want to comply that will be there problem. But they don't even do that.

    On a side note. I have stopped using the glimepiride and with the diet post hurricane without processed food I been able to control with LCHF diet alone. Maybe the glimepiride kicked my pancreas into action and it may not last. But it have been a few weeks since I stopped and my glucose levels are back to normal=(non-diabetic).

    That's good. Opinions vary on whether or if or when you can regrow beta cells but kicking down the insulin resistance can make those you have left more effective.
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    Post by chris c Mon Aug 06 2018, 23:31

    Long birder wrote:
    Interesting Graham for those of us who suspect we have low insulin diabetes and it is not caused directly by insulin resistance.  I suspect some reactive hypoglycemics may fall into that category?
    Another reason why we should all know our insulin profiles, but money is short and I can't see that happening.
    Interesting that this population can effectively take hyperinsulinemia out of the equation with CVD as the main cause! Do you read it like that?
    regards
    Derek

    I'd like to know for sure but I assume I have a lack of first phase insulin - hence the postprandial spikes - but still a good Phase 2 response, hence the later drops. On high carb I was probably hyperinsulinemic due to the IR.

    I'll read this one later, but AFAIK both high glucose and high insulin affect CVD risk through different pathways.
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    Post by graham64 Tue Aug 14 2018, 22:48

    Can't remember if this has been posted before or not 

    Study on the levels of glycosylated lipoprotein in patients with coronary artery atherosclerosis.

    Abstract
    BACKGROUND:
    The main risk factors for atherosclerosis patients are not fully explicated. The aim of this study was to analyze the levels of blood lipid and glycosylated lipoprotein in patients with coronary artery atherosclerosis and healthy individuals and to study the relationship between the glycosylated lipoprotein and atherosclerosis.

    METHODS:
    The study involved 200 patients diagnosed with myocardial infarction caused by coronary atherosclerosis as case group and 230 healthy individuals as control group. We analyzed and contrasted the levels of blood lipid and glycosylated lipoprotein between the different groups. In addition, we investigated the correlation between glycosylated low-density lipoprotein (G-LDL) and glucose levels.

    RESULTS:
    There is no statistical difference between the level of TG in case group and control group. The level of CHOL, HDL-C, and LDL-C in case group is significantly lower than that in control group (3.90 [3.23, 4.42] vs 5.16 [4.86, 5.77] [mmol/L]; 1.09 [0.83, 1.38] vs 1.46 [1.15, 1.80] [mmol/L]; 2.22 [1.68, 2.81] vs 2.95 [2.60, 3.27] [mmol/L]) (P < 0.05). The level of GLU, HbA1c, G-HDL, and G-LDL in case group is significantly higher than that in control group (7.10 [5.68, 9.27] vs 4.84 [4.68, 5.07] [mmol/L]; 6.8 [6.3, 7.4] vs 5.9 [5.6, 6.1] [%]; 30.08 [25.04, 40.17] vs 22.95 [18.14, 27.06] [ng/mL], 6.26 [4.95, 7.50] vs 3.61 [2.66, 5.15] [ng/mL]) (p < 0.05). The level of G-LDL in patients with coronary atherosclerosis was relevant with the level of GLU and HbA1c (r = 0.625, 0.706, P < 0.05), and there was no relevance with LDL-C (r = 0.331, P > 0.05).

    CONCLUSION:
    Hyperlipidemia is not an important cause of coronary atherosclerosis. High glucose levels and glycosylated lipoprotein are of high importance in the development and progression of coronary atherosclerosis.

    https://www.ncbi.nlm.nih.gov/pubmed/30101436
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    Post by chris c Fri Aug 17 2018, 23:36

    Here

    http://sci-hub.tw/https://doi.org/10.1002/jcla.22650

    no I hadn't already got that one so thanks and I'll read it later.

    meanwhile some more I have collected

    Countries’ geographic latitude and their human populations’ cholesterol and blood
    2 pressure

    https://www.biorxiv.org/content/early/2018/05/16/308726

    I wonder if another factor to the Vitamin D3 is also nitric oxide.

    Urinary sodium excretion, blood pressure, cardiovascular
    disease, and mortality: a community-level prospective
    epidemiological cohort study

    http://sci-hub.tw/10.1016/S0140-6736(18)31376-X

    Andrew Mente et al from PURE

    rather shows the ridiculousness of salt restriction unless you eat huge quantities - yet another U curve/J curve

    Hypercaloric Diets With Increased Meal Frequency,
    but Not Meal Size, Increase Intrahepatic
    Triglycerides: A Randomized Controlled Trial

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4265261/pdf/hep0060-0545.pdf

    "Conclusion: A hypercaloric diet with high
    meal frequency increased IHTG and abdominal fat independent of caloric content and
    body weight gain, whereas increasing meal size did not. This study suggests that snacking,
    a common feature in the Western diet, independently contributes to hepatic steatosis
    and obesity."

    Like most people LCHF has killed my need to snack.

    A randomized controlled-feeding trial based on the Dietary Guidelines
    for Americans on cardiometabolic health indexes

    https://academic.oup.com/ajcn/article/108/2/266/5067923

    "The consumption of a DGA dietary pattern for 8 wk without weight loss reduced systolic blood pressure. There were no differences between the DGA and TAD diets in fasting insulin, glucose, indexes of insulin resistance, or fasting lipids"

    so basically, the Dietary Guidelines For Americans wasn't any better than the standard crap diet. Nice to see proof.

    Vegetarian Diet Improves HbA1c, Reduces CV Risk in Diabetes

    https://www.medscape.com/viewarticle/898976

    That didn't go too well either, 0.29% reduction in A1c

    Lots of militant vegans in the comments though.

    Full paper here

    http://sci-hub.tw/10.1016/j.clnu.2018.05.032

    Outcomes of a Digitally Delivered Low-Carbohydrate Type 2
    Diabetes Self-Management Program: 1-Year Results of a
    Single-Arm Longitudinal Study


    https://asset.jmir.pub/assets/5b9b0a16e0e5e909fab15fe05e330d94.pdf

    David Unwin & co. That's the way to do it

    "Results: Of the 1000 study participants, 708 (70.80%) individuals reported outcomes at 12 months, 672 (67.20%) completed
    at least 40% of the lessons, and 528 (52.80%) completed all lessons of the program. Of the 743 participants with a starting HbA1c
    at or above the type 2 diabetes threshold of 6.5%, 195 (26.2%) reduced their HbA1c to below the threshold while taking no
    glucose-lowering medications or just metformin. Of the participants who were taking at least one hypoglycemic medication at
    baseline, 40.4% (289/714) reduced one or more of these medications. Almost half (46.40%, 464/1000) of all participants lost at
    least 5% of their body weight. Overall, glycemic control and weight loss improved, especially for participants who completed all
    10 modules of the program. For example, participants with elevated baseline HbA1c (≥7.5%) who engaged with all 10 weekly
    modules reduced their HbA1c from 9.2% to 7.1% (P<.001) and lost an average of 6.9% of their body weight (P<.001)."



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    Post by chris c Tue Aug 21 2018, 22:51

    Saturated Fat: Part of a Healthy Diet

    http://sci-hub.tw/10.1007/s13668-018-0238-x

    "Purpose of Review Despite the American public following recommendations to decrease absolute dietary fat intake and specifically
    decrease saturated fat intake, we have seen a dramatic rise over the past 40 years in the rates of non-communicable diseases
    associated with obesity and overweight, namely cardiovascular disease. The development of the diet-heart hypothesis in the mid
    twentieth century led to faulty but long-held beliefs that dietary intake of saturated fat led to heart disease. Saturated fat can lead to
    increased LDL cholesterol levels, and elevated plasma cholesterol levels have been shown to be a risk factor for cardiovascular
    disease; however, the correlative nature of their association does not assign causation.
    Recent Findings Advances in understanding the role of various lipoprotein particles and their atherogenic risk have been
    helpful for understanding how different dietary components may impact CVD risk. Numerous meta-analyses and systematic
    reviews of both the historical and current literature reveals that the diet-heart hypothesis was not, and still is not,
    supported by the evidence. There appears to be no consistent benefit to all-cause or CVD mortality from the reduction of
    dietary saturated fat. Further, saturated fat has been shown in some cases to have an inverse relationship with obesity-related
    type 2 diabetes.
    Summary Rather than focus on a single nutrient, the overall diet quality and elimination of processed foods, including simple
    carbohydrates, would likely do more to improve CVD and overall health. It is in the best interest of the American public to clarify
    dietary guidelines to recognize that dietary saturated fat is not the villain we once thought it was."

    The Militant Vegans disagree, obviously.

    Effect of combined use of a low-carbohydrate, high-protein diet with
    omega-3 polyunsaturated fatty acid supplementation on glycemic
    control in newly diagnosed type 2 diabetes: a randomized,
    double-blind, parallel-controlled trial

    http://sci-hub.tw/10.1093/ajcn/nqy120

    "Results: Compared with the CON diet group, greater decreases in
    glycated hemoglobin (HbA1c) and fasting glucose were observed in
    all of the other 3 diet groups at 12 wk. Of note, HbA1c reduction
    in the LCHP+ω-3 diet group (−0.51%; 95% CI: −0.64%, −0.37%)
    was greater than that in the LCHP (P = 0.03) and ω-3 (P = 0.01) diet
    groups at 12 wk. In terms of fasting glucose, only the LCHP+ω-3 diet
    group showed a significant decrease at 4 wk (P = 0.03 compared with
    CON). Moreover, the reduction in fasting glucose in the LCHP+ω-
    3 diet group (−1.32 mmol/L; 95% CI: −1.72, −0.93 mmol/L) was
    greater than that in the LCHP (P = 0.04) and ω-3 (P = 0.03) diet
    groups at 12 wk"

    Not perfect but interesting, hint: 42% carbs is NOT low.

    Effects of Popular Diets without Specific Calorie Targets on Weight Loss Outcomes: Systematic Review of Findings from Clinical Trials

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5579615/

    "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."

    Ooh the dieticians aren't going to like this.

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    Post by graham64 Wed Aug 22 2018, 22:18

    Have you noticed Chris just like these two many of the studies you put up have no COI's  no influence from pharma or food companies  Smile
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    Post by chris c Sat Aug 25 2018, 00:16

    graham64 wrote:Have you noticed Chris just like these two many of the studies you put up have no COI's  no influence from pharma or food companies  Smile

    Precisely! Also interesting to see the influences of veganism/vegetarianism/Seventh Day Adventists at work even when there are no financial conflicts. And of course there are hidden conflicts like ILSI being funded by Coke, etc.

    Thanks to Tom Naughton



    Michael Eades takes Peter at Hyperlipid's work on mitochondria and protons and translates it for us lesser mortals.

    As Peter Cleave said, it makes no sense for modern diseases to be caused by ancestral foods. The change in types of fat is a huge factor in modern diets.
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    Post by chris c Thu Aug 30 2018, 22:54

    More, mainly thanks to Medical Twitter and a few blogs

    Oxidative Priority, Meal Frequency, and the Energy Economy of Food and Activity: Implications for Longevity, Obesity, and Cardiometabolic Disease

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5326984/

    The Insulin Resistance Time Bomb

    https://www.hormonesmatter.com/insulin-resistance-time-bomb/

    Rapid Non-Enzymatic Glycation of the Insulin
    Receptor under Hyperglycemic Conditions Inhibits
    Insulin Binding In Vitro: Implications for
    Insulin Resistance

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5751205/

    something I did NOT previously know, not only the insulin receptors but insulin itself can be gklycated

    Problems with the 2015 Dietary Guidelines for Americans: An Alternative

    https://www.researchgate.net/publication/304181135_Problems_with_the_2015_Dietary_Guidelines_for_Americans_An_Alternative

    James Di Nicolantonio and Zoe Harcombe

    A 12-week, whole-food carbohydrate-restricted feasibility study in overweight children

    https://insulinresistance.org/index.php/jir/article/view/42

    short but sweet, from Caryn Zinn and Grant Schofield among others

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    Post by graham64 Mon Sep 03 2018, 22:07

    Spotted on twitter  Cool

    Association between insulin resistance and the development of cardiovascular disease

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

    Also more from Caryn Zinn

    Assessing the nutrient intake of a low-carbohydrate, high-fat (LCHF) diet: a hypothetical case study design 

    https://bmjopen.bmj.com/content/8/2/e018846
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    Post by graham64 Wed Sep 05 2018, 22:44

    Study on the levels of glycosylated lipoprotein in patients with coronary artery atherosclerosis.

    Abstract
    BACKGROUND:
    The main risk factors for atherosclerosis patients are not fully explicated. The aim of this study was to analyze the levels of blood lipid and glycosylated lipoprotein in patients with coronary artery atherosclerosis and healthy individuals and to study the relationship between the glycosylated lipoprotein and atherosclerosis.

    METHODS:
    The study involved 200 patients diagnosed with myocardial infarction caused by coronary atherosclerosis as case group and 230 healthy individuals as control group. We analyzed and contrasted the levels of blood lipid and glycosylated lipoprotein between the different groups. In addition, we investigated the correlation between glycosylated low-density lipoprotein (G-LDL) and glucose levels.

    RESULTS:
    There is no statistical difference between the level of TG in case group and control group. The level of CHOL, HDL-C, and LDL-C in case group is significantly lower than that in control group (3.90 [3.23, 4.42] vs 5.16 [4.86, 5.77] [mmol/L]; 1.09 [0.83, 1.38] vs 1.46 [1.15, 1.80] [mmol/L]; 2.22 [1.68, 2.81] vs 2.95 [2.60, 3.27] [mmol/L]) (P < 0.05). The level of GLU, HbA1c, G-HDL, and G-LDL in case group is significantly higher than that in control group (7.10 [5.68, 9.27] vs 4.84 [4.68, 5.07] [mmol/L]; 6.8 [6.3, 7.4] vs 5.9 [5.6, 6.1] [%]; 30.08 [25.04, 40.17] vs 22.95 [18.14, 27.06] [ng/mL], 6.26 [4.95, 7.50] vs 3.61 [2.66, 5.15] [ng/mL]) (p < 0.05). The level of G-LDL in patients with coronary atherosclerosis was relevant with the level of GLU and HbA1c (r = 0.625, 0.706, P < 0.05), and there was no relevance with LDL-C (r = 0.331, P > 0.05).

    CONCLUSION:
    Hyperlipidemia is not an important cause of coronary atherosclerosis. High glucose levels and glycosylated lipoprotein are of high importance in the development and progression of coronary atherosclerosis.

    https://www.ncbi.nlm.nih.gov/pubmed/30101436

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