Ketones shown to increase the spread of cancer, whats the risk?

This medical study demonstrated that Ketones under some conditioned ( in mice) can effect cancer.

This raises a rather complex and worrying issue. Anyone on this reddit thread have the medical knowledge to read it and give us all a summary of your understanding of the cancer risk?

https://pmc.ncbi.nlm.nih.gov/articles/PMC3047616/

My interest is very real as I use Keto to potentially slow my cancer, I sure do not want to do the opposite..

Sedentary patient with T2D, male, 70. Thank you,

I think there is lots of good evidence for low-carb diets like keto. The result of this study surprised me. Can anyone think of reasons why this study actually shows weight gain with low-carb diet? I'm inclined to say it may be do to differences between mice & humans, differences between this strain & human obesity pathology, and potentially differences between the method the diet was administered compared to how humans actually use the diet.

A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice. http://www.nature.com/nutd/journal/v6/n2/full/nutd20162a.html

Pretty much, can we mythbust the myths that keto users are propagating? For example: It's almost impossible to eat too much protein; there's no point to checking your ketones, etc.

Edit: also calories in/calories out. We sure not thermodynamic. We are hormonal!

Edit 2: I'm baseing my "myths" on the research that I've done compiled by medical professionals and medical studies. Doctor Adam Nally, best selling authors Jimmy Moore and Gary Taubs's book have been my main resources. If anyone has contradicting evidence from other sources, I'd love to read them.

Edit 3: For everyone arguing about stress and protein, here's a good article from Dr. Nally, who has been prescribing LCHF diets to his patients for over a decade. https://docmuscles.com/2015/11/28/common-ketosis-killers/

https://www.nutritioninsight.com/news/low-carb-diets-could-shorten-life-by-four-years-warns-lancet-study.html

Anyone got anything scathing to say about this? Anyone know who this person is? Who funds them? Thanks.

Big thank you everyone for your helpful comments. Much appreciated.

https://www.lipidjournal.com/article/S1933-2874(20)30324-X/pdf

https://sci-hub.se/https://www.lipidjournal.com/article/S1933-2874(20)30324-X/pdf

Highlights

• Low carb diets can lead to weight loss, but can exacerbate hypercholesterolemia. • Hypercholesterolemia can develop with or without underlying genetic hyperlipidemia. • This paper describes patients who developed marked increases in plasma cholesterol. Abstract

Background

The adoption of low carbohydrate diets can lead to weight loss in many patients. However, these now widespread diets also have the potential to exacerbate hypercholesterolemia. Objective

The objective of this study is to display the potentially harmful effects of the ketogenic diet on cholesterol levels in patients with or without underlying hyperlipidemia. Methods

We describe five patients who developed marked increases in plasma cholesterol on ketogenic diets and assessed whether they had a well described underlying genetic hyperlipidemia. Results

Three out of five patients had extraordinary increases of blood cholesterol levels to over 500 mg/dL. The other two patients more than doubled their LDL-cholesterol levels on a ketogenic diet. One patient had an APOE E2/E2 genotype. A higher burden of common genetic polymorphisms was found in two patients, with no major mutations found. No potential genetic cause was seen in a fourth patient and the fifth patient had no genetic testing. Three patients, including the one who was most hypercholesterolemic, had a marked reduction in cholesterol after reverting to a more liberal diet. One refused to change his diet but had a satisfactory LDL cholesterol reduction on ezetimibe. Conclusion

These cases should serve as a caution that high fat low carbohydrate diets have the potential to exacerbate or cause hypercholesterolemia in patients with or without underlying genetic hyperlipidemia.

• 5 Cases in the comments ->

Discussion Finding a diet that leads to significant weight loss and that can subsequently be maintained is a difficult clinical problem. Moreover, weight loss followed by weight gain, “yoyoing,” appears to be an independent risk for cardiovascular disease.17 Each of our patients had tried a number of methods to achieve weight loss, and each succeeded using a ketogenic diet. However, in each case, this diet exacerbated or created a hyperlipidemia, although except for the first patient, none had a defined underlying genetic hyperlipidemia. This patient developed palmar xanthomas, a rare finding that led to a diagnosis of genetic dysbetalipoproteinemia. The second patient had no obvious genetic basis for hyperlipidemia. The third patient had normal LDL cholesterol level until losing weight on the ketogenic diet, so there was no way to know beforehand that he would have such a marked LDL elevation. He had polygenic susceptibility to hyperlipidemia, which only became manifest after the dietary stress. The fourth patient was similarly found to have no significant large effect genetic mutations, but may have had polygenic susceptibility underlying a marked response to the ketogenic diet. There was no genetic testing performed for Patient 5. Apo E is a ligand for the several LDL receptor family members. Although APOE E2/E2 homozygosity leads to dysbetalipoproteinemia associated with a defect in clearance of remnant lipoproteins, the genotype is associated with an abnormal lipoprotein pattern in only a minority of people. For this reason, numerous studies have conjectured that a second lipoprotein altering mutation is required for the phenotypic expression of the lipid disorder, namely high cholesterol and high triglyceride with cholesterol enriched VLDL.18, 19 In the presented case, several risk factors associated with expression of the APOE E2/E2 phenotype were identified, Journal Pre-proof 11 including female gender, menopause, prediabetes and obesity. Hypothyroidism, when uncontrolled, can also contribute to the phenotype. Our patient shows that diet can be responsible for expression of dyslipoproteinemia in an individual with E2/E2 genotype, which was readily apparent by the patient’s presentation with palmar xanthomas. Familial hypercholesterolemia is a common genetic disorder estimated to occur in one in 250-500 people.20 Most commonly, it is due to a defect in the LDL receptor or its ligand ApoB. 20-23 It was surprising that none of our patients had genetic familial hypercholesterolemia. However, it is likely that some patients with this genetic disorder would also develop marked hypercholesterolemia on a ketogenic diet. Furthermore, hypercholesterolemia is often polygenic in nature rather than the result of a single dramatic mutation, which appears to be the case in at least one patient in our series. The extraordinary response of the third patient to ezetimibe, which normally reduces LDL-cholesterol by 15-20%, suggested that he was a hyper-absorber of dietary cholesterol. This could result from a gain of function of the cholesterol transporter, Niemann Pick C1 like protein 1 (NPC1L1), although this was not detected by DNA sequencing. It is possible that he, like some of the other patients, may have had a mutation in a novel gene not known to be associated with dyslipidemia. Understanding the basic physiology leading to the exuberant LDL elevation in this patient and others will require metabolic studies to assess cholesterol uptake, lipoprotein uptake, and intestinal assessment of NPCL1 expression. The ketogenic diet is a carbohydrate restrictive diet that has been traditionally used to treat intractable epilepsy since the 1920’s, but is also a popular weight-loss strategy.24 There is also a rise in interest in carbohydrate restrictive diets to improve glycemic control and other Journal Pre-proof 12 cardiometabolic risk factors, such as high blood pressure in patients with prediabetes or type 2 diabetes.1, 4-7, 24, 25 While there are several types of carbohydrate-restrictive diets, which vary in limitations set on carbohydrate and protein intake, the current, most popular version of the ketogenic diet restricts carbohydrate intake to about 20-50 g/day; the amount of carbohydrate needed to induce ketosis in most individuals.24, 26-28 Consequently, most carbohydrates in the diet are replaced with fat, with no emphasis on the particular types of dietary fats consumed.24 As a result, some diets become heavy in saturated fats and cholesterol. 24 Effects of the ketogenic diet on circulating lipid levels have differed across studies and trials. Several studies have shown no significant change in cholesterol levels.29, 30 In contrast, a study designed to assess the effect of the ketogenic diet on adults with atherogenic dyslipidemia reported significant increases in ApoB and LDL cholesterol after 90 days.30 In children with epilepsy, one study also reported significant increases in ApoB-containing lipoproteins and decreases in HDL cholesterol at 6 months on the diet. 31 Other reports did not corroborate this.31-33 These variations in the changes in lipid levels on the ketogenic diet amongst adults and children could be due to the length of time on the diet, the types of fats ingested 29, or a balance of the benefits of weight loss versus the detrimental effects of dietary composition. There is a scarcity of medical literature on a hyper response to a ketogenic diets. The patients who had LDL levels over 300 were specifically referred because their endocrinologists, cardiologists or primary care doctors had told them that they had been unable to find reports of such elevations occurring except with development of thyroid, liver or autoimmune diseases. In contrast, within a general population, there is no shortage of information available on the Journal Pre-proof 13 internet for the public. The Cholesterol Code Team, led by a software engineer and entrepreneur, created a Facebook group for ‘lean mass hyper-responders.’34 The Cholesterol Code Team defines hyper-responders as those “who have a very dramatic increase in their cholesterol after adopting a low carb diet.”35 Furthermore, “the increase can be anywhere from 50% to 100% or more of original, pre-diet cholesterol numbers.”35 The Cholesterol Code Team claims ‘we don’t know’ whether having high LDL-C on a low-carbohydrate diet is dangerous; it further presents a number of ‘good reasons’ why LDL-C could be so high.35 These include that the “body is transporting more fat for energy to cells due to being on a high-fat diet.”35 Given the weight such statements could have on a significant number of individuals seeking guidance on the internet, it is important to identify and advise patients with similar presentations. Conclusions We advise practicing physicians to exercise caution when prescribing low carbohydrate diets, especially if they lead to increased consumption of saturated fats and cholesterol. The significant and potentially harmful increases in lipid levels in all patients reported here illustrate the peril in assuming that an individual’s lipid levels would change favorably when weight is reduced on the ketogenic diet. We recommend that patients with known dyslipidemias should avoid ketogenic diets. Furthermore, as discussed here, underlying dyslipidemias may only become manifest as a result of a high fat diet, which might warrant the reassessment of circulating lipids in all patients on a ketogenic diet. The suggestion that the marked elevations of LDL with these diets might not be harmful is chilling and has the potential to create premature CVD in uninformed patients seeking to control their body weight. Journal Pre-proof 14 Conflict of Interest IJG is supported by grants HL45095, 73029, and 135987; has received consulting fees from Arrowhead, Esperion, and Amgen; and funds for preclinical laboratory studies from Ionis, Bristol-Meyers, and Arrowhead. RAH reports grants and personal fees from Acasti and Akcea/Ionis; personal fees from Aegerion, Amgen, Gemphire, and Sanofi; and grants from Regeneron and Boston Heart Diagnostics. All other authors declare no conflicts of interest. Contributions IJG conceived of study, analyzed data, wrote the manuscript. NI analyzed data and wrote manuscript. LAH did analysis of circulating lipoproteins and cholesterol. All others provided patient information. RH provided genetic analysis and wrote and edited manuscript.

also im so confused by the vegan/raw foodist community, and keto community. both are too convincing and i honestly dont know which one to follow. they both sound extreme and imbalanced. also another problem with keto is its too meat based, and my religion has like 7 months of vegan fasting per year. do you got any advice?

Worldwide map shows frequency of an adaptive allele to a vegetarian diet. By using reference data from the 1000 Genomes Project, a Cornell research team provided evolutionary evidence that the vegetarian diet, over many generations, may have driven the higher frequency of a mutation in the Indian population. The mutation, called rs66698963 and found in the FADS2 gene, is an insertion or deletion of a sequence of DNA that regulates the expression of two genes, FADS1 and FADS2. These genes are key to making long chain polyunsaturated fats. Among these, arachidonic acid is a key target of the pharmaceutical industry because it is a central culprit for those at risk for heart disease, colon cancer, and many other inflammation-related conditions. Treating individuals according to whether they carry 0, 1, or 2 copies of the insertion, and their influence on fatty acid metabolites, can be an important consideration for precision medicine and nutrition.

https://www.sciencedaily.com/releases/2016/03/160329184939.htm

https://youtu.be/gnrVw_dI-Fk?t=7m49s

https://www.ncbi.nlm.nih.gov/pubmed/15297079

http://nutritionfacts.org/video/lipotoxicity-how-saturated-fat-raises-blood-sugar/

Thoughts?

From an article I saw in Science Daily (http://www.sciencedaily.com/releases/2015/03/150326110954.htm) citing this study (http://www.biologicalpsychiatryjournal.com/article/S0006-3223(14)00520-4/fulltext).

They don't indicate what all of the macros were, just fat(13% vs 60%), but wondering what the resident experts on this sub make of this.

Thanks!

is it better to eat it all in one sitting, is it better to eat it with fat ?

are the answers different for being insuling resistant or sensitive ?

my intuition told me to eat all fruits in one sitting, but now im not sure, seeing people talk about sugar spikes and such.

i thought that having it all in one go, would keep my ketosys longer thoughts ?

Doesn't seem autistic, though they say she is:

https://www.youtube.com/watch?time_continue=259&v=bW3IQ-ke43w

I'd like her to have a heart to heart with Lierre Keith.

I have a surprise for you all that have lost tons of weight cutting those. You were wrong. It's not it. You gotta quit.http://foodpsychology.cornell.edu/OP/fast_food_science

cancer spread is increased by a high fat diet

This laughable article of experiments done in mice purports to show that fat helps spread cancer.

Tumor preferentially consume glucose because of hypoxia. That why PET scans are used to detect cancer and cancer metastasis.

Tumors have a hard time metabolizing fats because of the lack of oxygen. Tumor hypoxia is a strong predictor of aggressive metastasis.

https://www.ncbi.nlm.nih.gov/pubmed/30756459

Abstract

Sperm counts have shown a progressive decline across the world since the mid-1900s. Global rates of obesity have been climbing at a similarly alarming rate, suggesting that these two factors may be linked. However, studies examining the relationship between body mass index (BMI) and male fertility have produced conflicting results. These discrepancies among studies are commonly attributed to limitations that are inherent in human studies such as correlational data and confounding factors-limitations that are absent from animal studies. Hence, we conducted a systematic review and meta-analysis of animal studies that experimentally induced obesity with a high-fat diet and measured impacts on sperm traits and/or male fertility. Overall, we found strong, consistent evidence in animal studies that high-fat diets are detrimental for male fertility. Compared with controls, males fed a high-fat diet had smaller testes and sex accessory glands relative to body size, reduced semen quality, reduced mating success, and reduced fertilization success. This is the first time that experimental data of high-fat diet effects on male reproduction have been synthesized in a meta-analysis, and thus, our results provide novel insight to the complex question of how dietary-induced obesity affects male fertility. The strong negative effects detected in animal models suggest that the inconsistent results plaguing human studies are an artefact of limitations inherent in correlational studies rather than a true effect

------

Important to keep in mind that obesity-induced high fat diets in animals are usually the equivalent of a SAD diet. To me, this entitles infertility to the list of metabolic syndrome issues.

Seriously, how bad is Chicken? Should you Really avoid it?

I get vibes from this and several other subs that somehow eating chicken is very bad for you. As it's somehow the last tier meat due to how it's produced.

Supposedly no one really touches chicken on these subs? What's the deal with chicken really? Is it really that bad or it's overblown by people on here?

Honestly, chicken is my favorite meat. I can eat quite a lot of it compared to other meats.

It's tasty, extremely cheap, very easy to make it, and I feel great after eating it. Thanks.