Sibiriak

Literature review: Meal Timing & Blood Sugar (June 21, 2021)

Thanks. Flegal got some pretty vicious and arguably unfair push back on her shocking conclusion that " overweight [not obesity] was associated with significantly lower all-cause mortality. " Not surprising, really. Established public health policy was under attack. And big money at stake. “Studies such as Flegal's [2013] are dangerous, Willett says, because they could confuse the public and doctors, and undermine public policies to curb rising obesity rates. ‘There is going to be some percentage of physicians who will not counsel an overweight patient because of this,’ he says. Worse, he says, these findings can be hijacked by powerful special-interest groups, such as the soft-drink and food lobbies, to influence policy-makers.” Debate raged on Flegal's controversial work back in 2013, and now, eight years later, she seems to want to stir things up again, or at least set the record straight from her perspective. Of course, the science has moved steadily on since then, as we have discussed here in various threads such as: Relationship Between BMI and Disease, and Longevity Optimal Weight for Longevity

24?

Well, maybe 23 then. 😊 I bet you'd look ripped.

Here's my simplistic take: For most people, not all: if you eat a WFPB diet, keep your calories low, animal proteins low, saturated fats low, simple sugars low, and exercise, you shouldn't have much trouble achieving healthy cholesterol and glucose levels. The relative amounts of healthy carbs and fats is probably the least important variable. Dean Pomerleau (2016): In your case, McCoy, the first thing I'd suggest would be to reduce your caloric intake, bringing your BMI down to the 20-22 range. (Yeah, I know all the contrary bodybuilding arguments...)

I saw that coming! We already know, of course, that IGF-1 is a double-edged sword. In any case, the 2013 study posted by Mike L is a narrowly-focused modified-mouse study that makes no claim about optimal IGF-1 serum levels in humans. It's not directly comparable to the 2020 human study I posted.

Insulin-like Growth Factor-1 and IGF Binding Proteins Predict All-Cause Mortality and Morbidity in Older Adults (2020) https://www.mdpi.com/2073-4409/9/6/1368/htm

Btw, a full text of the key study cited by Greger can be found here: Effects of dietary supplementation with creatine on homocysteinemia and systemic microvascular endothelial function in individuals adhering to vegan diets https://crearene.com/wp-content/uploads/2021/04/R-Bavel_et_al-2019-Fundamental__Clinical_Pharmacology.pdf A few excerpts: For those who haven't seen the video: Greger suggests that vegans who still have high homocysteine levels (> 10 μmol/L) even wtih B12 supplementation (eg. 2000 mcg cyanocobalamin/ wk) consider taking 1 g/day high-purity creatine as an empirical experiment.

With all due respect, you seem to be attacking the source of an argument, rather than the argument itself-- a very unscientific tactic. More importantly, there doesn't appear to be any scientific consensus when it comes to the origin of the Covid-19 virus. Or rather, if there is a consensus it is that BOTH the natural-origin and lab-origin hypotheses are plausible. Media blackout Right now, almost all of the arguments being made are about the plausibility of one hypothesis compared to another. But plausibility is not evidence. And it doesn't look like we are going to get any decisive concrete evidence very soon on this question. So politics will continue to dominate. 1.The origin of COVID: Did people or nature open Pandora’s box at Wuhan? Nicholas Wade, May 5, 2021. "[Jonathan Cook:] Nicholas Wade, a former New York Times science writer, set out in May, in an in-depth investigation, why the case for a lab leak was scientifically strong, citing some of the world’s leading virologists. But Wade also highlighted a much deeper problem for US elites: just before the first outbreak of Covid, the Wuhan lab was, it seems, cooperating with the US scientific establishment and WHO officials on its virus experiments – what is known, in scientific parlance, as “gain-of-function” research." 2. Investigate the origins of COVID-19, Science, 14 May 2021. " In May 2020, the World Health Assembly requested that the World Health Organization (WHO) director-general work closely with partners to determine the origins of SARS-CoV-2 (2). In November, the Terms of Reference for a China–WHO joint study were released (3). The information, data, and samples for the study's first phase were collected and summarized by the Chinese half of the team; the rest of the team built on this analysis. Although there were no findings in clear support of either a natural spillover or a lab accident, the team assessed a zoonotic spillover from an intermediate host as “likely to very likely,” and a laboratory incident as “extremely unlikely” [(4), p. 9]. Furthermore, the two theories were not given balanced consideration. Only 4 of the 313 pages of the report and its annexes addressed the possibility of a laboratory accident (4). Notably, WHO Director-General Tedros Ghebreyesus commented that the report's consideration of evidence supporting a laboratory accident was insufficient and offered to provide additional resources to fully evaluate the possibility (5). As scientists with relevant expertise, we agree with the WHO director-general (5), the United States and 13 other countries (6), and the European Union (7) that greater clarity about the origins of this pandemic is necessary and feasible to achieve. We must take hypotheses about both natural and laboratory spillovers seriously until we have sufficient data. A proper investigation should be transparent, objective, data-driven, inclusive of broad expertise, subject to independent oversight, and responsibly managed to minimize the impact of conflicts of interest. Public health agencies and research laboratories alike need to open their records to the public. Investigators should document the veracity and provenance of data from which analyses are conducted and conclusions drawn, so that analyses are reproducible by independent experts." .

Interesting question. I hope someone else chimes in here with a comprehensive response. I'm too lazy at the moment to attempt one myself. Just a couple of points. 1) There's seems to be a general consensus that the calcium/magnesium ratio is as important as absolute intake amounts (as it is with other minerals such as zinc/copper etc.). Unfortunately, there is still a lot of disagreement about optimal intake levels and ratios. See, for example Calcium for Vegans and other threads. 2) Testing for calcium/magnesium biomarkers (serum, urine) may or may not provide useful information. The following article is primarily focused on low magnesium intake, but has a lot of general information which may be relevant to your question. Essential Nutrient Interactions: Does Low or Suboptimal Magnesium Status Interact with Vitamin D and/or Calcium Status?

I agree 100%. That was my reaction exactly.

Global trends in clinical studies of ivermectin in COVID-19 http://jja-contents.wdc-jp.com/pdf/JJA74/74-1-open/74-1_44-95.pdf Excerpt: See also: “I Don’t Know of a Bigger Story in the World” Right Now Than Ivermectin: NY Times Best-Selling Author (May 25, 2021) It’s Time To Talk About Ivermectin (March 30, 2021)

POLL: Most Americans now believe the coronavirus originated from a laboratory in China

Exercise—A Panacea of Metabolic Dysregulation in Cancer: Physiological and Molecular Insights (2021) Int J Mol Sci. 2021 Apr; 22(7): 3469. PMID: 33801684 Steffen H. Raun,1Kristian Buch-Larsen,2,3Peter Schwarz,2,3 and Lykke Sylow1,4,* . Figure 2 Cancer is associated with adverse changes of metabolic important tissues, including skeletal muscle (myocytes), adipose tissue (adipocytes), and the liver (hepatocytes). Those changes include insulin resistance, hyperlipidemia, mitochondria dysfunction, inflammation, and muscle mass loss (cancer cachexia) and there is significant tissue crosstalk. Abbreviations: ATGL; adipose triglyceride lipase, HSL; hormone sensitive lipase, ROS; reactive oxygen species. Figure 3 Illustration of the temporal metabolic benefits of exercise and molecular mechanisms. (A) One exercise bout elicits an acute and transient increase in muscle glucose uptake that is independent of insulin and persists in insulin-resistant subjects. (B) Insulin sensitivity (illustrated here as insulin-stimulated glucose uptake) is transiently enhanced for up to 48 h after the last exercise bout. (C) Repeated exercise training leads to longer-term adaptations, including increased expression of fat- and glucose-handling proteins and increased capillarization that improves insulin sensitivity and elevates muscle fat- and glucose-handling capacity. Abbreviations: AMP-activated protein kinase, FA; fatty acid, RAC1; Ras-related C3 botulinum toxin substrate 1, ROS, reactive oxygen species, TBC1D1; TBC1 Domain Family Member 1. 5. Unanswered Questions The following knowledge gaps hinder optimal treatment of metabolic dysfunction in cancer and hamper our ability to harness the beneficial effects of exercise: The optimal exercise regimen for benefitting metabolic regulation in cancer remains to be established. The appropriate implementation of exercise into the oncological treatment of cancer must be determined. It is important to establish whether an acute exercise bout fully stimulates insulin-independent glucose uptake into the exercising muscles in cancer patients. This will be vital information in the daily life for cancer patients, as improved glycemic control is associated with the effectiveness of cancer treatment and improved survival. It would have real-life patient benefits to determine whether the insulin-sensitizing effect of one bout of exercise exists in patients with cancer and can be exploited in relation to the timing between exercise and meals to maximize glucose disposal, reduce hyperinsulinemia, and elevate muscle protein synthesis. For cancer patients with cancer cachexia, it is important to determine whether exercise can treat the loss of muscle mass and improve strength and which exercise regimen is most effective. Deeper knowledge of the molecular mechanisms by which exercise benefits metabolic regulation is needed to identify novel therapeutically drug targets. This is especially important in patients with cancer cachexia who are unlikely to easily exercise [260]. 6. Conclusions The evidence is clear that dysregulated metabolism is a common feature of cancer. It manifests as peripheral insulin resistance, hyperlipidemia, mitochondrial dysfunction, inflammation, and cachexia. Contemporary observational studies have shown that cancer survival depends on better metabolism management strategies, as metabolic dysfunctions are associated with reduced survival and increased cancer recurrence risks for most cancers. Exercise produces acute as well as longer-term metabolic benefits by improving insulin sensitivity, restoring hyperlipidemia, reducing inflammation, enhancing mitochondrial function, and increasing muscle mass and strength. Thus, exercise could be an important strategy to improve metabolic function in cancer but randomized controlled trials in patients with cancer are warranted. The American College of Sports Medicine updated its exercise guidelines for cancer treatment of a variety of cancer health-related outcomes including fatigue, anxiety, depression, sleep, function, and quality of life [261]. Improved metabolic regulation could likely be added to that list in the future, yet, current evidence is limited and many exciting discoveries lie ahead.

We interrupt this discussion for a important censorship announcement from Facebook: “In light of ongoing investigations into the origin of Covid-19 and in consultation with public health experts, we will no longer remove the claim that Covid-19 is man-made from our apps.” “We’re continuing to work with health experts to keep pace with the evolving nature of the pandemic and regularly update our policies as new facts and trends emerge." Thank you for your cooperation. Carry on.