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[–] [email protected] 2 points 14 hours ago* (last edited 14 hours ago)

Notes from the paper:

All participants were asked to stay on a KD during their follow-up, and to measure adherence, 3 dietary recalls and daily b-hydroxybutyrate (bHB) data were collected using the Automated Self-Administered 24-Hour (ASA24) Dietary Assessment Tool from the National Institutes of Health. Blood bHB monitoring devices by KetoMojo (Napa) were provided to each participant.

Look at that, they verified ketone state!

with 87% of the cohort recording values above >=0.3 mmol/L on a majority of measurements, a threshold chosen given the known steady-state drop in circulating ketone levels with prolonged adaptation

However, this does not mean that the LMHR population is without risk. The observed, the observed PAV progression in this KETO-CTA cohort was comparable to what has been observed in other studies on populations with lower LDL-C across the cardiovascular disease risk spectrum. It should be emphasized that this includes heterogeneity in progression (and regression) across the population

despite profound elevations in LDL-C and ApoB, based on these data, LMHR subjects with CAC 0 at baseline (n 57) constitute a low-risk group for PAV progression, even as compared to other cohorts with far lower LDL-C and ApoB. By contrast, LMHR subjects with elevated baseline CAC, possibly from a history of metabolic damage and dysfunction prior to adopting a CRD, appear to constitute a relatively higher risk group for PAV progression even where LDL-C and ApoB are equal to their CAC counterparts.

the dropout rate was 0%, and adherence to the KD was assessed by dietary records and bHB measurements

For these 100 people the KD was sustainable

[–] [email protected] 2 points 14 hours ago* (last edited 7 hours ago)

Dave Feldman (author) did a tiny presentation: https://youtu.be/HJJGHQDE_uM

Dr Scher also covers it https://www.youtube.com/watch?v=RSGj6UJusTg

Nick Norwitz (author) does a big video presentation of this: https://youtu.be/a_ROZPW9WrY

If you prefer a written summary: https://staycuriousmetabolism.substack.com/p/big-news-the-lean-mass-hyper-responder

100 people, prospective study, with plaque imaging, a very strong signal.

TLDR: the Lean Mass Hyper Responders (LMHR) following a ketogenic diet with high LDL do not show a growth in plaque over the period of 1 year. 6 people showed a reduction in plaque.

  • Most participants showed no or minimal progression of coronary plaque

  • Neither ApoB nor LDL exposure predicted plaque progression

While both LDL-C and ApoB are independent risk factors for atherosclerosis, the absolute risk associated with elevated LDL-C and ApoB is CONTEXT-DEPENDENT, including the etiology (cause) of the elevations in these biomarkers, LDL-C and ApoB as well as interactions with other risk markers, like insulin resistance

high LDL-C and ApoB among a metabolically healthy population have different cardiovascular risk implications than high LDL-C among those with metabolic dysfunction.

  • Elevations in LDL-C and ApoB are dynamic and result from a metabolic response to carbohydrate restriction, rather than as a function of a genetic defect. These people aren’t born with high LDL, it’s a response to carbohydrate restriction having to do with energy flux through the body.

  • These participants are of normal-health weight (BMI <25 kg/m2) and metabolically healthy rather than living with obesity, pre-diabetes or type 2 diabetes or other insulin resistance disorders.

  • The high LDL-C and ApoB in this phenotype emerge as part of a lipid triad, also inclusive of high HDL-C and low triglycerides, representing a metabolic signature of a distinct physiological state.

 

TLDR - If you are a ketogenic lean mass hyper responder with high LDL, insist on imaging to determine your atherosclerotic risk, as this study indicates the LDL and ApoB by itself doesn't indicate a growth in plaque.

Background - Changes in low-density lipoprotein cholesterol (LDL-C) among people following a ketogenic diet (KD) are heterogeneous. Prior work has identified an inverse association between body mass index and change in LDL-C. However, the cardiovascular disease risk implications of these lipid changes remain unknown.

Objectives - The aim of the study was to examine the association between plaque progression and its predicting factors.

Methods - One hundred individuals exhibiting KD-induced LDL-C ≥190 mg/dL, high-density lipoprotein cholesterol ≥60 mg/dL, and triglycerides ≤80 mg/dL were followed for 1 year using coronary artery calcium and coronary computed tomography angiography. Plaque progression predictors were assessed with linear regression and Bayes factors. Diet adherence and baseline cardiovascular disease risk sensitivity analyses were performed.

Results - High apolipoprotein B (ApoB) (median 178 mg/dL, Q1-Q3: 149-214 mg/dL) and LDL-C (median 237 mg/dL, Q1-Q3: 202-308 mg/dL) with low total plaque score (TPS) (median 0, Q1-Q3: 0-2.25) were observed at baseline. Neither change in ApoB (median 3 mg/dL, Q1-Q3: −17 to 35), baseline ApoB, nor total LDL-C exposure (median 1,302 days, Q1-Q3: 984-1,754 days) were associated with the change in noncalcified plaque volume (NCPV) or TPS. Bayesian inference calculations were between 6 and 10 times more supportive of the null hypothesis (no association between ApoB and plaque progression) than of the alternative hypothesis. All baseline plaque metrics (coronary artery calcium, NCPV, total plaque score, and percent atheroma volume) were strongly associated with the change in NCPV.

Conclusions - In lean metabolically healthy people on KD, neither total exposure nor changes in baseline levels of ApoB and LDL-C were associated with changes in plaque. Conversely, baseline plaque was associated with plaque progression, supporting the notion that, in this population, plaque begets plaque but ApoB does not. (Diet-induced Elevations in LDL-C and Progression of Atherosclerosis [Keto-CTA]

Full Paper: https://doi.org/10.1016/j.jacadv.2025.101686

[–] [email protected] 1 points 17 hours ago

https://en.wikipedia.org/wiki/Tim_Noakes

1,2 - Expert opinion will differ, and pillorying someone for expressing their opinion seems uncharitable.

3 - Fat Diet : This entire community is about the science behind Low Carb, the papers he publishes are about Low Carb. This is the place to talk about that diet.

4- Professional Reprimands - You mean the South African accreditation trial where he was proven correct? we spoke of that before https://hackertalks.com/post/5813954

5- Scams? What scams?

His academic publications speak for themselves: https://scholar.google.com/citations?hl=en&user=sZnJQoQAAAAJ&view_op=list_works&sortby=pubdate

However, the corner stone of science is reproducibility not authority - I'm happy to talk about any science you have indicating his publications are wrong

11
Get Out - 2017 (en.wikipedia.org)
 

A really excellent film, that deserves thought and reflection

Jared Bauer does a excellent breakdown : 8 years later, i finally understand get out https://youtu.be/NW38mJ1DqPE

[–] [email protected] 1 points 17 hours ago (2 children)

Why is Noakes a quack? What is your definition?

[–] [email protected] 1 points 18 hours ago

We already covered the paper they reference in this interview: https://hackertalks.com/post/7986045

 

Summary

In this episode of the KetoPro Podcast, Richard Smith welcomes back Professor Tim Noakes to discuss the impact of low carbohydrate diets on athletic performance. They explore recent research findings that challenge traditional beliefs about carbohydrates and muscle glycogen, emphasizing the importance of blood glucose levels during endurance activities. The conversation also addresses the adaptation process for athletes transitioning to low carb diets, the health implications of dietary choices for athletes, and the evolving landscape of sports nutrition. In this conversation, the speakers delve into the implications of carbohydrate consumption on athletic performance and overall health. They discuss the hidden dangers of high carbohydrate diets, the efficiency of fat as a fuel source, and the body's macronutrient needs. Personal experiences with zero carb diets are shared, along with insights into the future of research in this area. The conversation also touches on the addiction to carbohydrates among athletes and the genetic factors influencing performance. Ultimately, the speakers advocate for a shift in dietary practices to enhance health and athletic longevity.

Takeaways

  • The low carb diet is gaining traction in various sports.
  • Carbohydrates can enhance performance, but only during prolonged exercise.
  • Muscle glycogen depletion is not as critical as previously thought.
  • A small amount of glucose can improve endurance performance.
  • Blood glucose levels play a significant role in athletic performance.
  • Many studies fail to account for adaptation periods in low carb diets.
  • Elite athletes may not always be the best model for dietary studies.
  • Health concerns are rising among athletes consuming high carb diets.
  • The shift towards low carb diets in sports is inevitable.
  • Individual performance improvements matter more than comparisons with elite athletes. High carbohydrate diets can lead to insulin resistance.
  • Fat can provide the majority of energy needed for endurance sports.
  • The human body is capable of burning fat efficiently.
  • Glucose is essential for brain function during exercise.
  • Zero carb diets can lead to improved athletic performance.
  • Athletes often consume excessive carbohydrates unnecessarily.
  • Genetics play a significant role in athletic performance.
  • Addiction to sugars is prevalent among athletes.
  • Long-term health benefits from a low-carb lifestyle are significant.
  • Research on zero carb athletes is needed to understand their performance.

Chapters

00:00 Introduction and Guest Welcome
01:40 Exploring Carbohydrates and Athletic Performance
03:04 Research Insights on Low Carb Diets
09:10 The Role of Carbohydrates in Endurance Sports
10:10 Debating Muscle Glycogen vs. Blood Glucose
17:23 Adaptation and Supplementation in Low Carb Diets
20:13 Comparing Elite and Amateur Athletes
28:02 Health Implications of Diet in Athletes
32:00 The Hidden Dangers of High Carbohydrate Diets
34:48 The Efficiency of Fat as Fuel
36:14 Understanding the Body's Macronutrient Needs
37:59 The Role of Glucose in Endurance Sports
39:45 Personal Experiences with Zero Carb Diets
42:05 The Future of Zero Carb Research
45:27 The Impact of Diet on Athletic Performance
48:00 The Addiction to Carbohydrates
50:56 The Genetic Factors in Athletic Performance
53:16 The Importance of Resilience in Endurance Sports

summeraizer

In this episode of the KetoPro Podcast, Richard Smith talks with Professor Tim Noakes about the role of low-carb diets in sports. They discuss Noakes' latest research, which offers insights into how carbohydrates influence athletic performance, particularly in endurance sports. The conversation highlights how the average athlete may not require excessive carbohydrates, and successful performance can be achieved on low-carb or fat-adapted diets.

Key Points

Carbohydrates and Athletic Performance

Professor Noakes discusses whether carbohydrates are necessary for enhancing athletic performance. His research indicates that carbs do boost performance but primarily during prolonged exercise when blood glucose levels drop.

Low-Carb Diets in Sports

Noakes mentions that one of the top coaches in a sport believes low-carb diets will become standard, reflecting a growing acceptance of such diets among athletes.

Research Findings on Fat Utilization

The research conducted by Noakes and his team shows that high-fat diets do not compromise endurance performance. In various trials, athletes maintained their performance levels on low-carb diets, emphasizing fat as a preferred fuel source.

Glucose's Role During Exercise

The discussion reveals that only small amounts of glucose are needed during prolonged exercise to prevent hypoglycemia rather than to fuel muscle metabolism.

Impact of Diet on Health and Performance

The episode underscores the relationship between diet and health, with low-carb diets shown to improve blood glucose control and overall health metrics, potentially extending athletes' careers.

Cultural and Psychological Barriers to Diet Change

Noakes and Smith talk about the addiction to carbohydrates in both amateur and elite athletes, explaining how societal norms influence dietary habits.

Future of Nutritional Practices in Sports

Professor Noakes predicts a shift towards carnivore and low-carb diets in professional sports as more evidence emerges in support of these diets.

[–] [email protected] 1 points 19 hours ago

Back to normal food now

[–] [email protected] 2 points 20 hours ago

The reviews are not great, but the real question is will it hit a billion dollars?

I wonder how many kids will watch the movie multiple times?

[–] [email protected] 1 points 21 hours ago* (last edited 21 hours ago)

Not me, I think it's a great idea....

I have no idea how such impossible projects get greenlit... Is it just a bluffing game that nobody expects to actually finish so everyone keeps upping the ante?

[–] [email protected] 3 points 21 hours ago* (last edited 20 hours ago)

I still think this form of top posting is content jacking and stealing engagement from green engineering who posted in the other community

[–] [email protected] 7 points 23 hours ago

This is what happens when we let algorithms become our nannies

 

https://www.chriscookingnashville.com/recipe-cards?cardid=4743726915108

  • 227 g cream cheese (softened)
  • 57 g melted butter
  • 9.86 ml white vinegar
  • 30 g pork panko (or other meat flour)
  • 108 g whey protein (or beef isolate)
  • 6 g egg white powder
  • 59 g butter powder
  • 21 g unflavored gelatin
  • 2-4 Tbsp allulose (optional; can be subbed for another keto sweetener to taste)
  • 1 large whole egg
  • 2 egg yolks (or a second whole egg)
  • 2 g baking soda
  • 2-3 Tbsp cubed butter
  • Beef tallow, lard, ghee, bacon grease, or other animal fat for coating baking dish
16
submitted 1 day ago* (last edited 1 day ago) by [email protected] to c/[email protected]
 

We saw The Minecraft Movie! Correction: we saw A Minecraft Movie. This movie is a Minecraft movie, because someone had to make it. It stars Jack Black because of course it does. In the film, lights and colors appear on the screen and people in the audience laugh when characters say that their butt hurts. It is truly a magical time at the cinema and we can only hope that this Minecraft Movie is not the only Minecraft Movie.

https://en.wikipedia.org/wiki/A_Minecraft_Movie

Jeremy Jahns "Temu Jumanji" https://youtu.be/hhj16SqR-Yc

 

Thomas N. Seyfried received his Ph.D. in Genetics and Biochemistry from the University of Illinois, Urbana, in 1976. He did his undergraduate work at the University of New England, where he recently received the distinguished Alumni Achievement Award. He also holds a Master’s degree in Genetics from Illinois State University. Thomas Seyfried served with distinction in the United States Army’s First Cavalry Division during the Vietnam War and received numerous medals and commendations. He was a Postdoctoral Fellow in the Department of Neurology at the Yale University School of Medicine and then served on the faculty as an Assistant Professor in Neurology.

Other awards and honours have come from such diverse organisations as the American Oil Chemists Society, the National Institutes of Health, The American Society for Neurochemistry, the Ketogenic Diet Special Interest Group of the American Epilepsy Society, the Academy of Comprehensive and Complementary Medicine, and the American College of Nutrition.

Dr. Seyfried previously served as Chair, Scientific Advisory Committee for the National Tay-Sachs and Allied Diseases Association and presently serves on several editorial boards, including those for Nutrition & Metabolism, Neurochemical Research, the Journal of Lipid Research, and ASN Neuro, where he is a Senior Editor.

Dr. Seyfried has over 150 peer-reviewed publications and is the author of the book, Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer (Wiley, 1st ed., 2012).

Summarizer

In this presentation, Professor Thomas Seyfried discusses the concept of cancer as a metabolic disease rather than a genetic one. He argues that the prevailing view of cancer being primarily caused by genetic mutations fails to address the fundamental issue of mitochondrial dysfunction. Seyfried presents evidence that highlights the significant role of metabolism in cancer development and provides insights into novel therapeutic strategies focused on metabolic management. His work suggests that shifting the understanding of cancer could lead to more effective and less toxic treatment options.

Key Points

Current cancer crisis overview

Seyfried opens by presenting statistics from the American Cancer Society that highlight the alarming increase in cancer cases and deaths, pointing out that there has been little progress in reducing cancer mortality over the years.

Cancer as a metabolic disease

He introduces the idea that cancer should be primarily viewed as a mitochondrial metabolic disease, suggesting that damage to mitochondria leads to mutations in the nuclear DNA, which are secondary effects rather than primary causes of cancer.

Critique of somatic mutation theory

Seyfried challenges the dominant belief that cancer is a genetic disease caused by mutations in DNA. He argues that the focus on genetic mutations has shaped medical approaches to cancer treatment and that this perspective has failed to lead to meaningful progress in curing cancer.

Evidence supporting mitochondrial theory

Through various research studies and experiments, Seyfried illustrates that cancer cells possess dysfunctional mitochondria, which leads to altered energy metabolism, primarily dependent on fermentation instead of oxidative phosphorylation.

The Warburg effect and metabolic reprogramming

He discusses the Warburg effect, where cancer cells prefer to generate energy through fermentation even in the presence of oxygen and highlights the need for therapies that target the metabolic pathways of cancer cells.

Proposed therapeutic strategies

Seyfried proposes strategies for managing cancer that focus on lowering glucose and glutamine levels while promoting the usage of ketone bodies, suggesting a shift in the cancer treatment paradigm towards metabolic approaches.

Press-pulse therapy

He introduces a new therapeutic approach called press-pulse therapy, which combines chronic stress on cancer metabolism with acute interventions aimed at synergistically targeting cancer cells, aiming for improved patient health without the toxic effects of traditional treatments.

Need for a paradigm shift in cancer treatment

Seyfried concludes by emphasizing that recognizing cancer as a mitochondrial metabolic disease rather than a genetic one may revolutionize cancer therapy, leading to more effective and less harmful treatment options.

Publication List https://scholar.google.com/citations?user=ctSRQrsAAAAJ

Here is the paper the talk is largely based from : https://doi.org/10.3389/fcell.2015.00043 - Cancer as a mitochondrial metabolic disease

Here is the proposed press-pulse protocol : https://pubmed.ncbi.nlm.nih.gov/28250801/ - Press-pulse: a novel therapeutic strategy for the metabolic management of cancer

Here is a application of that protocol for glioblastomas : https://pubmed.ncbi.nlm.nih.gov/39639257/ - Clinical research framework proposal for ketogenic metabolic therapy in glioblastoma

 

The American Heart Association is supposed to work to prevent heart disease, the #1 killer worldwide. Surprisingly, the AHA openly opposed the SNAP reform bill, which would prevent the purchase of junk food with SNAP. Is the American Heart Association really trying to keep us on a “heart-healthy” diet? Find out in this video.

Summarizer

Dr. Eric Berg discusses the American Heart Association's surprising opposition to a bill in Texas aimed at restricting food stamp purchases of unhealthy foods like soda and candy. Despite the AHA's mission to prevent heart disease, they expressed concerns about participation in the SNAP program and the economic implications of the bill. The video exposes conflicts of interest between the AHA and the junk food industry, highlighting significant taxpayer subsidies to the soda industry that contribute to health issues such as obesity and diabetes. Berg argues for the need to shift SNAP funding toward healthier food options to reduce chronic disease and healthcare costs.

Key Points

AHA's Opposition to SNAP Bill

The American Heart Association opposed a Texas bill aimed at restricting food stamps for unhealthy foods. This opposition surprised many, as the AHA's primary mission is to prevent heart disease, which is linked to the consumption of sugary drinks and junk food.

Industry Influence on AHA

Dr. Berg highlights that the AHA receives significant funding from the junk food industry, raising concerns about conflicts of interest. The association's industry partnerships, such as the industry nutrition forum, illustrate the financial ties between them and large food corporations.

Economic Impact of Soda Subsidies

The video notes that taxpayers subsidize the soda industry through SNAP at a staggering $10 billion annually. This funding promotes the purchase of unhealthy foods, contributing to obesity and related health problems, thereby benefiting the big food and pharmaceutical industries.

Call for SNAP Reform

Dr. Berg advocates for reforming SNAP to support only nutrient-dense foods instead of processed options. Such changes could decrease the burden of chronic illnesses and reduce healthcare spending by fostering healthier eating habits among low-income individuals.

Junk Food Industry's Strategies

The soda industry’s campaign against the SNAP bill includes hiring social media influencers and using arguments around food freedom and insecurity to maintain their profits. This highlights a broader PR battle over health and nutrition policy.

 

Nutrition Epidemiology is a branch of pseudoscience. In this discussion, Prof Kay provides 7 major flaws (each of which are sufficient on their own) to invalidate and discredit nutrition epidemiology and nutrition epidemiologists as fantasists, pseudoscientists, and crackpots. These pseudoscientists have abandoned scientific discipline, and instead indulge in criminal propaganda. Check it out! Don't forget to subscribe, and hit the bell icon. Also leave me your thoughts.

Summarizer:

In this video, Professor Bart Kay argues that nutrition epidemiology is flawed and misleading due to seven main invalidating issues. He emphasizes that association does not imply causality, discusses problems with observational studies, and highlights biases in data collection and reporting that result in false conclusions about health outcomes related to nutrition.

Key Points

Association vs Causation

Professor Kay stresses that simply having an association between two variables does not prove that one causes the other. He gives the example of ice cream sales correlating with shark attacks, illustrating the fallacy of assuming causality from correlation.

Observational Study Limitations

Nutrition epidemiology relies on observational studies which lack control over variables affecting health outcomes. The inability to conduct controlled experiments limits the validity of conclusions drawn from these studies.

Respondent Data Issues

Epidemiological studies often depend on self-reported dietary data, which can be biased or inaccurate. People may misreport their food intake, leading to flawed conclusions.

Arbitrary Selection Criteria in Meta-analyses

Authors of meta-analyses can selectively include or exclude studies based on arbitrary criteria, potentially biasing outcomes to support a desired conclusion.

Publication Bias

Studies that yield negative or inconclusive results are less likely to be published, skewing the available literature and leading to inflated positive results in meta-analyses.

P-Hacking in Research

Researchers may manipulate data collection to achieve statistically significant results (p < 0.05), which can misrepresent the actual findings and contribute to flawed reports.

Misuse of Relative Outcomes

Epidemiological studies often report relative risks without presenting absolute risks, which can mislead the public regarding the actual impact of dietary choices on health.

Extrapolation of Findings

Findings from studies often conducted on older populations are generalized to the entire population, ignoring individual health variations and leading to inappropriate dietary recommendations.

4
submitted 3 days ago* (last edited 3 days ago) by [email protected] to c/[email protected]
 

Video: https://www.youtube.com/watch?v=RaMPCuYZ208

In this video, Professor Bart Kay debunks ten common claims associated with carnivore, asserting that they are misrepresented or unfounded. He discusses cholesterol and its association with heart disease, saturated fats, the necessity of fiber, and the supposed benefits of vegetable sources of Vitamin C. Each point is backed by scientific data and studies, leading to the conclusion that vegan propaganda lacks solid scientific merit.

Key Points

Cholesterol myths

Kay argues that cholesterol is not a causal factor in heart disease, citing studies that show lower mortality rates associated with higher cholesterol levels in populations.

Saturated fat misconceptions

Multiple meta-analyses consistent in showing that saturated fat intake does not increase the risk of heart disease, contradicting common vegan narratives.

Fiber intake

Evidence from a study shows that removing fiber from the diet can improve symptoms of idiopathic constipation, challenging the assertion that fiber is essential for digestive health.

Vitamin C requirements

Vitamin C can be obtained adequately from animal sources, and excess intake could potentially lead to harmful oxalate production.

Trimethylamine oxide (TMAO) theory

Kay dismisses claims that TMAO from meat consumption is harmful, arguing that our bodies adapt to metabolize it without adverse effects.

Red meat and mortality association

He points out that studies linking red meat to increased mortality are primarily epidemiological and do not establish causation.

Blue Zones fallacies

Kay critiques the idea of Blue Zone diets supporting longevity, noting confounding factors like caloric intake and physical activity.

Teeth and dietary classification

Critiques the argument about teeth for determining diet, emphasizing that human dietary evolution involved significant meat consumption.

Epidemiology flaws

Discusses the numerous problems with using epidemiological studies to draw dietary conclusions, labeling much of the data as pseudoscientific.

References

  1. BHF, Cholesterol vs. Mortality statistics, 2005.
  2. doi: 10.1016/j.ahj.2008.08.010
  3. doi: 10.1080/17512433.2018.1519319
  4. Hooper L, et al. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Systematic Review, 2015. Results: The study found no effects of reducing saturated fat in heart attacks, strokes, or all-cause deaths.
  5. De Souza RJ, et al. Intake of saturated and trans unsaturated fatty acids and risk of all-cause mortality, cardiovascular disease, and type 2 diabetes: Systematic review and meta-analysis of observational studies. BMJ, 2015 Results: Saturated fat intake was not linked with heart disease, stroke, type 2 diabetes, or dying of any cause.
  6. Siri-Tarino PW, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition, 2010. Results: Saturated fat intake was not linked to an increased risk of cardiovascular disease, heart attacks, or strokes, even among those with the highest intake.
  7. Chowdhury R, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk: A systematic review and meta-analysis. Annals of Internal Medicine Journal, 2014. Results: The study did not find any link between saturated fat consumption and the risk of heart disease or death.
  8. Schwab U, et al. Effect of the amount and type of dietary fat on risk factors for cardiometabolic risk factors, and risk of developing type 2 diabetes, cardiovascular diseases, and cancer: A systematic review. Food and Nutrition Research, 2014. Results: Consuming saturated fat was not linked to an increased risk of heart disease or an increased risk of type 2 diabetes.
  9. youtube.com/watch?v=DEx9foeADnc [Dr Paul Mason Video]
  10. dx.doi.org/10.3748/wjg.v18.i33.4593.
  11. youtube.com/watch?v=8rK7vT6zfFs&pp=0gcJCR0AztywvtLA
  12. youtube.com/watch?v=DadUBmrFI78
  13. youtube.com/watch?v=LN5gcLz8tic
  14. youtube.com/watch?v=hq-JowK9T1w
  15. youtube.com/watch?v=zdSTxmo9aUo
  16. youtube.com/watch?v=qWgH-VaqMjQ
  17. doi: 10.2016/0140-6736(90)91656-u
  18. cdn.mdedge.com/files/s3fs-public/Document/September-2017/JFP_06307_Article1.pdf
 

Introduction: For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit.

Areas covered: The authors of three large reviews recently published by statin advocates have attempted to validate the current dogma. This article delineates the serious errors in these three reviews as well as other obvious falsifications of the cholesterol hypothesis.

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.

Full Paper: https://doi.org/10.1080/17512433.2018.1519391

 

Dr Penny Figtree graduated from the University of Sydney in 1993 with first class honours. With over 20 years in general practice she has now decided to focus on weight loss and diabetes.

This decision was made after seeing the power of a low carbohydrate diet to help people lose weight and for some to even reverse diabetes. Dr Figtree had previously tried to help patients using various diets such as low fat diets, Optifast, the 5:2 fast but nothing really worked. In the end she would just say “as long as you are not gaining weight then that’s great”. Then Dr. Figtree read a book called “Always Hungry” By Professor David Ludwig where he explained the INSULIN CARBOHYDRATE MODEL OF OBESITY.

Dr. Figtree has now been practising low carb medicine for several years. She describes this as the most rewarding part of her career, stopping medications and patients feeling well.

Summarizer

Dr. Penny Figtree discusses the use of continuous glucose monitors (CGMs) in healthy individuals, emphasizing their benefits and addressing concerns about their use. She explains how CGMs provide real-time glucose data, helps in understanding metabolic health, and might reveal undiagnosed conditions. The talk also touches on the controversies surrounding CGM use and practical advice for interpreting glucose readings.

Key Points

Introduction to Continuous Glucose Monitors

Dr. Figtree introduces continuous glucose monitors (CGMs), specifically the Freestyle Libre and Dexcom G6, highlighting how they measure blood glucose levels in real-time, providing valuable information for individuals to understand their metabolic health.

Controversy Over CGMs in Healthy Individuals

The use of CGMs in healthy people has sparked debate, with some experts arguing there is insufficient data to endorse their use outside of diabetic care. Dr. Figtree encourages individuals to consider CGMs as tools for gaining insights into their blood sugar responses and overall health.

Setting Up Alarm Parameters

Dr. Figtree advises users to set custom limits in the CGM app to avoid unnecessary alarm reactions. She explains the differences between sensor readings and blood glucose measurements, emphasizing not to panic over minor fluctuations.

Understanding Glucose Variations

The speaker explains that normal glucose responses can vary with exercise, food intake, and other factors. Healthy individuals usually maintain glucose levels below 7.8 mmol/L, but it's normal for levels to fluctuate occasionally.

Reactive Hypoglycemia Insights

Dr. Figtree discusses reactive hypoglycemia, where blood sugar drops significantly post-meal, often causing discomfort. She shares her experience with dietary changes and suggests increasing protein intake to mitigate this issue.

Dawn Phenomenon in Healthy Individuals

The early morning increase in glucose levels, known as the 'dawn phenomenon,' is explained as a natural hormonal response that can influence glucose readings in both diabetics and healthy individuals.

Potential Benefits of Using CGMs

Recent studies suggest that healthy adults may benefit from CGMs to monitor their glucose responses to various foods, which can help in identifying patterns and reducing risks associated with glucose variability.

Conclusion on CGM Usage

Dr. Figtree concludes that while CGMs can be beneficial for healthy individuals, it is essential to interpret the data appropriately and understand personal metabolic responses.

3
submitted 4 days ago* (last edited 4 days ago) by [email protected] to c/[email protected]
 

Not intentionally. Stressful week, unplanned traveling around. Ended up doing dirty carnivore.

Ordering bunless burgers from restaurants, with seed oils I'm sure. That was my main food source.

Hard boiling eggs in a water heater.

What have you been eating?

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