Sugar Feeds Thyroid

SugarFeedsThyroid “Starving an animal with a tumor increases the stress hormones, providing free fatty acids and amino acids, and accelerates the tumor’s growth…it’s impossible to “starve a tumor,” by the methods often used. Preventing the excessive breakdown of protein and reducing the release of fatty acids from fat cells would probably cause many cancer cells to die, despite the availability of glucose…” Ray Peat Phd

The idea that ‘sugar feeds cancer’ is very popular and has in recent times been heavily promoted. As a result of this, many people have been convinced that it would be wise to remove sugar from their diet altogether.

Experimental evidence, however, continues to show that not only is this not correct, but that to do so is dangerous, and can result in the creation of the kind of stressful conditions which promote the growth and spread of cancer (and its initial onset), and the development of many other diseases of stress and inflammation.

“…results support the proposal that an increase in availability of free fatty acids and/or ketone bodies is the stimulus that increases the rate of tumor growth during an acute fast.”

“…our current observations may also explain the close and emerging association between diabetes and cancer susceptibility…diabetes and fasting/starvation…are known to be highly ketogenic and…consistent with our current hypothesis that ketone production fuels tumor growth.”

Not long after removing sugar from your diet – and when glycogen stores have been depleted – there is an increase in the release of the stress related hormones (cortisol and adrenaline), as well as the liberation of greater amounts of stored fat into circulation (as free fatty acids in the blood), in an attempt by the body to provide the fuel necessary for survival.

In order to replace the sugar previously being eaten, fat consumption is often increased. So called ketogenic (or high fat low carb) diets, have become popular, and it is common to hear it suggested that such an approach is useful for the prevention (as well as even for the treatment) of cancer.

But unfortunately it looks like it isn’t as simple as that, as evidence has shown that cancer does not require you to be consuming sugar, in order for it to develop, and for it to thrive.

“Cancer cells undergo metabolic reprogramming in order to produce biosynthetic precursors, such as ATP, lipids, nucleotides and amino acids, which are required to sustain the energy and substrate demands for rapid growth and proliferation…lipid metabolism emerges as a critical pathway for the maintenance of cell survival, growth and migration…”

“…given our current findings that ketones increase tumor growth, cancer patients and their dieticians may want to re-consider the use of a “ketogenic diet” as a form of anti-cancer therapy.”

Increased ketone production in the body occurs under conditions of metabolic stress (and starvation), conditions which have been shown to ‘fuel’ the growth and metastasis of cancerous tumors.

Rising levels of cortisol (and other related stress substances), as well as the increased storage, and subsequent release of fat, into the blood (in particular the polyunsaturated fats or PUFAs), have been demonstrated in their own right to promote cancer development.

“…HF-LC diet increased whole-body regeneration of cortisol by 11β-HSD1 and reduced the rate of inactivation of cortisol…”

“We conclude that increased arterial blood plasma linoleic acid concentrations, caused by increased dietary intakes, specifically stimulate growth, lipid storage and linoleic acid metabolism in hepatoma…in vivo.”

Both cortisol and the polyunsaturated free fatty acids encourage inflammation, as well as the rise in release of other inflammatory cancer promoting biochemical substances, such as serotonin, prolactin, estrogen and nitric oxide.

“Recently it has been fully demonstrated that estrogens are carcinogenic in the human breast by testing in an experimental system the natural estrogen 17beta-estradiol (E(2))…”

“…studies have demonstrated that angiogenesis was the foundation for tumor growth and that NO [nitric oxide] is one of the most secondary messengers and is capable of promoting the process…”

“Data…available on serotonin involvement in cancer cell migration, metastatic processes and as a mediator of angiogenesis…Serum serotonin level was found to be suitable for prognosis evaluation of urothelial carcinoma in the urinary bladder, adenocarcinoma of the prostate and renal cell carcinoma.”

All of these (and other) stress substances, are known to interfere with energy metabolism, suppressing thyroid function and digestion, promoting bacterial overgrowth and endotoxin release, as well as increasing lactic acid production.

“Our data indicate that sustained LPS [endotoxin] accumulation represents a pathological mediator of inflammation-associated hepatocellular carcinoma…”

“Recent data suggest that the metabolic switch toward deregulation of glycolysis may be an early and fundamental event in tumorigenesis…accumulation of lactate in solid tumors is a pivotal and early event in the development of malignancies.”

When thyroid metabolism and digestion is slowed, intestinal barrier function is reduced, and this allows excess bacteria as well as endotoxin (and other harmful substances), to pass into the blood stream, placing stress on the liver – interfering with detoxification – and eventually helping to create a chronic and systemic state of inflammation, and interference with cellular function.

Increasing levels of lactic acid are a direct consequence of this kind of stressed metabolic state – where sugar is not being provided in sufficient quantity, or is unable to be properly utilized by the cell – and lactate production is an important process in the development of the ‘cancer metabolism’.

“Lactate is probably the only metabolic compound involved and necessary in all main sequela for carcinogenesis, specifically: angiogenesis, immune escape, cell migration, metastasis and self-sufficient metabolism.”

Sugar consumption (for instance sucrose and fructose) assists thyroid function – and directly suppresses cortisol – protecting against the excessive release from storage (and breakdown) of the polyunsaturated fats – helping to reduce inflammation – eventually lowering levels of the stress and cancer promoting hormones.

“Free fatty acids arachidonic acid and linoleic acid and their metabolites…were an estimated 1.8- to 3.3-fold greater in 37 patients with adenocarcinoma vs 111 patients without cancer…Serum fatty acids and their metabolites demonstrate good sensitivity and specificity for the identification of adenocarcinoma of the lung.”

“…we identify neutrophils as the main component and driver of metastatic establishment within the (pre-)metastatic lung microenvironment…Neutrophils have a fundamental role in inflammatory responses…we find that neutrophil-derived leukotrienes aid the colonization of distant tissues by selectively expanding the sub-pool of cancer cells that retain high tumorigenic potential.”

Sugar and its cortisol lowering effects, directly protect against the breakdown of muscle tissue, and the excessive release of certain amino acids – such as tryptophan, glutamine, methionine and cysteine – which can then become another factor intimately involved in enabling the spread and growth of cancer.

“Glutamine dependence is a prominent feature of cancer metabolism, and here we show that melanoma cells, irrespective of their oncogenic background, depend on glutamine for growth.”

“…various mechanisms through which tryptophan metabolites cause carcinogenesis…It could be concluded that tryptophan metabolites play a complementary role in promoting carcinogenesis…”

“Restriction of methionine may be an important strategy in cancer growth control particularly in cancers that exhibit dependence on methionine for survival and proliferation…”

Although many ‘fad’ diets have a reputation for fast weight loss, much of this appears to be the result of muscle wasting, and the rapid release of stored fat into the bloodstream, both of which damage metabolism, and promote and reflect the conditions demonstrated to be necessary for the onset of cancer, as well as inflammatory disease in general.

“The finding that amino acids together contribute the majority of cell mass is in agreement with the notion that cells are composed primarily of protein…the importance of rapid glycolysis and glutaminolysis for proliferating cells lies in an ability to generate metabolic products beyond biomass carbon.”

Even though cortisol has the potential to (at least in the short term) help provide a certain amount of symptom relief and energy substitution, in the longer term when levels are chronically rising due to issues associated with metabolic stress, this kind of ‘benefit’ tends to be unsustainable, promoting more stress, degeneration, aging and eventually disease.

“Chronic stress induces signalling from the sympathetic nervous system (SNS) and drives cancer progression…Here we show that chronic stress restructures lymphatic networks within and around tumours to provide pathways for tumour cell escape…”

A number of studies have shown that the consumption of sugar has decreased rather than risen, over the last few decades.

“Over the last half century in the United States, dietary LA [linoleic acid] intake has greatly increased as dietary fat sources have shifted toward polyunsaturated seed oils such as soybean oil…adipose tissue LA has increased by 136%…”

Environmental carcinogens – including radiation as well as toxic (and estrogenic) chemicals and poisons – have become ubiquitous. These factors, in combination with a very large increase in consumption of the polyunsaturated fats (and the addition of numerous other poisonous ingredients added to foods), and exposure to many other lifestyle stressors, are some of the most likely factors to be causing the rising incidence of cancer and related degenerative diseases.

Sugar helps to promote the production and effective use of cholesterol, and cholesterol (in combination with thyroid hormone and vitamin A) is a fundamental building block for the protective anti-cancer hormones – pregnenolone, progesterone, testosterone and DHEA – and is a basic anti-stress substance. Low cholesterol has been shown to be involved in the development of cancer.

Alternatively, stress and thyroid suppression can increase cholesterol production, and interfere with proper conversion, promoting increased levels in the blood, and greater exposure to conditions which promote the oxidation of cholesterol. This interference with metabolism can probably explain much of the association between high cholesterol and cancer.

Although I’m not a doctor (and none of this is intended as medical advice), from a genuinely biological perspective, it looks like sugar restriction not only does not protect against cancer, but instead can speed up its development, encourage its growth, and worsen outcomes.

“Altered cellular metabolism is a hallmark of cancer…exosomes act as a source of metabolite cargo carrying lactate, acetate, amino acids, TCA cycle intermediates, and lipids; and these metabolites are utilized by recipient cancer cells for proliferation…”

“…our results indicate that metastasis-initiating cells particularly rely on dietary lipids to promote metastasis.”

The substances which rise when sugar is restricted – including cortisol, adrenaline, lactic acid, nitric oxide, estrogen, serotonin and the polyunsaturated free fatty acids – also play a significant role in the development of other inflammatory disease states including insulin resistance and diabetes, NAFLD and cardiovascular disease.

A diet limiting overall fat intake, and including sufficient protein (from skim milk and gelatin) as well as plenty of sugar from sweet, ripe, juicy fruits, fruit juice, honey and white sugar, is one reasonable approach to lowering exposure to cortisol, polyunsaturated free fatty acids, lactate, harmful amino acids, as well as other inflammatory substances, and might one day be popularly accepted, as being an important part of a scientifically rational approach to protection, from the spread of cancer and related diseases.

“Lifestyle factors, including diet, play an important role in the survival of cancer patients…we show that a high-fat ketogenic diet…enhanced tumor growth potential…providing insights into the design of conceptualized “precision diets” that may prevent or delay tumor progression…”

“…we have demonstrated that pharmacologic inhibition of FAO [fatty acid oxidation] inhibited proliferation and sensitized human leukemia cells…to apoptosis induction…which supports the notion that fatty acids promote cell survival…results support the concept of FAO inhibitors as a therapeutic strategy”

Some things which have been shown to be helpful include pregnenolone, progesterone, aspirin, caffeine, niacinamide, vitamin A, DHEA, testosterone, vitamin C, glycine, tetracycline and some other antibiotics, coconut oil, cyproheptadine, activated charcoal, cascara, vitamin E, vitamin K, sodium bicarb, urea, red light, methylene blue, and other anti-stress substances.

It’s one thing to say that sugar feeds cancer, because in some sense it does. Sugar is fuel for cells. But the consumption of sugar certainly has not been shown to be responsible for the existence of cancer, nor does it appear to be behind the growth and spread of cancer. This has been confirmed in many scientifically valid ways. Even if we pretend for a second that sugar is to blame, if you take sugar away, it will ‘miraculously’ still be there, only this time it will bring trouble.

I would not be exaggerating if I said I was horrified, by how many people have been convinced that removing sugar from their diet is a good idea when they are unwell, as well as by how much good quality science contradicting that suggestion, is regularly being ignored.

“Since nutrient-limiting conditions are not uncommon during cancer development, we are interested in what pathways or which fuels might provide alternative sources for energy production in starved cancer cells…This finding indicates that liver cancer cells consume ketone bodies as a convenient fuel to promote survival and progression under stressed conditions.”

The idea that one should attempt to replicate conditions, which occur in the body as a result of stress and starvation, to protect against and treat diseases, which are the product of chronic stress, is more than just problematic.

But unfortunately there are many ways to reduce symptoms (at least in the short term), or biochemical markers related to a disease, in order to make it look like you have improved a persons health, when in fact all that you often have done, is increased susceptibility to inflammation and stress, and encouraged conditions which promote the development and spread of cancer and other inflammatory diseases.

This kind of ‘cut, burn, poison and starve’ approach, is unlikely to go away, whilst the dominant view of cancer is that it is a genetically driven disease of the cell, rather than what it has arguably been proven to be, a systemic inflammatory metabolic stress illness.

There are plenty of good quality scientific reasons to wonder why the alternative approach, which suggests promoting stress free healthy metabolic function, rarely gets a mention in the medical world, regardless of the fact that it is well supported and far more logical.

So just try to remember, sugar also feeds thyroid, and it feeds the liver, and it feeds metabolic function in general, and when these things are working well, cancer is nowhere to be found.

See more here

Ketones and lactate increase cancer cell “stemness”, driving recurrence, metastasis and poor clinical outcome in breast cancer

Ketones and lactate “fuel” tumor growth and metastasis

Hyperketonemia (ketosis), oxidative stress and type 1 diabetes

Hormonal regulation of ketone-body metabolism in man.

Ketone body utilization drives tumor growth and metastasis

Tumor microenvironment derived exosomes pleiotropically modulate cancer cell metabolism

Lactate: A Metabolic Key Player in Cancer

Prevention of Dietary-Fat-Fueled Ketogenesis Attenuates BRAF V600E Tumor Growth

Polyunsaturated fatty acids mobilize intracellular Ca2+ in NT2 human teratocarcinoma cells by causing release of Ca2+ from mitochondria

Acute stress persistently enhances estrogen levels in the female rat.

Role of Hyperketonemia in Inducing Oxidative Stress and Cellular Damage in Cultured Hepatocytes and Type 1 Diabetic Rat Liver.

Possible roles of excess tryptophan metabolites in cancer.

An aberrant SREBP-dependent lipogenic program promotes metastatic prostate cancer

Hyperketonemia and ketosis increase the risk of complications in type 1 diabetes

Is low cholesterol a risk factor for cancer mortality?

Serotonin and cancer: what is the link?

Prolactin and cancer: Has the orphan finally found a home?

Stimulation of tumor growth in adult rats in vivo during an acute fast.

Ketone bodies and two-compartment tumor metabolism.

End-tidal CO2 levels lower in subclinical and overt hypothyroidism than healthy controls; no relationship to thyroid function tests

Hyperketonemia increases tumor necrosis factor-alpha secretion in cultured U937 monocytes and Type 1 diabetic patients and is apparently mediated by oxidative stress and cAMP deficiency.

A review of methionine dependency and the role of methionine restriction in cancer growth control and life-span extension.

Hypothalamic sensing of ketone bodies after prolonged cerebral exposure leads to metabolic control dysregulation

High Fat Diet Alters Lactation Outcomes: Possible Involvement of Inflammatory and Serotonergic Pathways

The role of estrogen in the initiation of breast cancer.

Dietary fats and cancer.

Fibroblast growth factor receptor is a mechanistic link between visceral adiposity and cancer

Induction of low-T3 syndrome in exercising women occurs at a threshold of energy availability.

Effect of hyperketonemia (Acetoacetate) on nuclear factor-κB and p38 mitogen-activated protein kinase activation mediated intercellular adhesion molecule 1 upregulation in endothelial cells.

Effect of hyperketonemia on plasma lipid peroxidation levels in diabetic patients.

Long term exposure to fatty acids and ketones inhibits B-cell functions in human pancreatic islets of Langerhans.

Function of inducible nitric oxide synthase in the regulation of cervical cancer cell proliferation and the expression of vascular endothelial growth factor

Inflamed tumor-associated adipose tissue is a depot for macrophages that stimulate tumor growth and angiogenesis.

Diabetic ketoacidosis increases extracellular levels of the major inducible 70-kDa heat shock protein.

Dietary fat and breast cancer.

Dietary linoleic acid intake controls the arterial blood plasma concentration and the rates of growth and linoleic acid uptake and metabolism in hepatoma 7288CTC in Buffalo rats.

Gene expression profiling of prostate tissue identifies chromatin regulation as a potential link between obesity and lethal prostate cancer.

Ketosis leads to increased methylglyoxal production on the Atkins diet.

Blood ketone bodies in congestive heart failure.

Pharmacologic inhibition of fatty acid oxidation sensitizes human leukemia cells to apoptosis induction

Increase in Adipose Tissue Linoleic Acid of US Adults in the Last Half Century

Inhibition of fatty acid oxidation as a therapy for MYC-overexpressing triple-negative breast cancer

Plasma level of LDL-cholesterol at diagnosis is a predictor factor of breast tumor progression

Sudden cardiac death in association with the ketogenic diet.

Association of Ketone Body Levels With Hyperglycemia and Type 2 Diabetes in 9,398 Finnish Men

Adipocytes promote ovarian cancer metastasis and provide energy for rapid tumor growth

Stromal Progenitor Cells from Endogenous Adipose Tissue Contribute to Pericytes and Adipocytes That Populate the Tumor Microenvironment

Direct evidence of iNOS-mediated in vivo free radical production and protein oxidation in acetone-induced ketosis

Dietary therapy is not the best option for refractory nonsurgical epilepsy.

Hepatocellular carcinoma redirects to ketolysis for progression under nutrition deprivation stress

PHD3 Loss in Cancer Enables Metabolic Reliance on Fatty Acid Oxidation via Deactivation of ACC2

Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance

Rise of ketone bodies with psychosocial stress in normal weight men.

Adipocyte p62/SQSTM1 Suppresses Tumorigenesis through Opposite Regulations of Metabolism in Adipose Tissue and Tumor

Endotoxin accumulation prevents carcinogen-induced apoptosis and promotes liver tumorigenesis in rodents.

Complications of the ketogenic diet.

Warburg Meets Autophagy: Cancer-Associated Fibroblasts Accelerate Tumor Growth and Metastasis via Oxidative Stress, Mitophagy, and Aerobic Glycolysis

Arachidonic acid and docosahexaenoic acid supplemented to an essential fatty acid-deficient diet alters the response to endotoxin in rats.

mTORC2 Promotes Tumorigenesis via Lipid Synthesis

Omentum and bone marrow: how adipocyte-rich organs create tumour microenvironments conducive for metastatic progression.

Serum Free Fatty Acid Biomarkers of Lung Cancer

Vegetable Oils Consumption as One of the Leading Cause of Cancer and Heart Disease

Pancreatic stellate cells support tumour metabolism through autophagic alanine secretion

Elevated polyunsaturated fatty acids in blood serum obtained from children on the ketogenic diet.

Acute pancreatitis causing death in a child on the ketogenic diet.

The fat and the bad: Mature adipocytes, key actors in tumor progression and resistance

Reexamining cancer metabolism: lactate production for carcinogenesis could be the purpose and explanation of the Warburg Effect

The Ketogenic Diet Alters Endocrine Regulation of Energy Metabolism in Ultra-Endurance Athletes

Tumor growth in patients with tuberous sclerosis complex on the ketogenic diet.

Ras Involvement in Signal Transduction by the Serotonin 5-HT2B Receptor

Glutamate and asparagine cataplerosis underlie glutamine addiction in melanoma

A ketogenic diet accelerates neurodegeneration in mice with induced mitochondrial DNA toxicity in the forebrain

Blood nutrient concentrations and tumor growth in vivo in rats: relationships during the onset of an acute fast.

Control of Nutrient Stress-Induced Metabolic Reprogramming by PKCζ in Tumorigenesis

Vascular effects of a low-carbohydrate high-protein diet

Chronic stress in mice remodels lymph vasculature to promote tumour cell dissemination

Amino acids rather than glucose account for the majority of cell mass in proliferating mammalian cells

Cardiac complications in pediatric patients on the ketogenic diet.

Chronic cellular hypoxia as the prime cause of cancer: what is the de-oxygenating role of adulterated and improper ratios of polyunsaturated fatty acids when incorporated into cell membranes?

The lipolysis pathway sustains normal and transformed stem cells in adult Drosophila

Neutrophils support lung colonization of metastasis-initiating breast cancer cells

Dietary Macronutrient Content Alters Cortisol Metabolism Independently of Body Weight Changes in Obese Men

Ketone body production and disposal in diabetic ketosis. A comparison with fasting ketosis.

Life-threatening complications of the Atkins diet?

Fatty acid oxidation is required for the respiration and proliferation of malignant glioma cells

FoxA and LIPG endothelial lipase control the uptake of extracellular lipids for breast cancer growth

Hepatic steatosis, inflammation, and ER stress in mice maintained long term on a very low-carbohydrate ketogenic diet.

Some hormonal influences on glucose and ketone body metabolism in normal human subjects.

Targeting metastasis-initiating cells through the fatty acid receptor CD36

The role of fatty acid β-oxidation in lymphangiogenesis

Low-carbohydrate ketogenic diets, glucose homeostasis, and nonalcoholic fatty liver disease.

A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain.


Image: Poster for Anti-Isis “International Daesh Cartoon and Caricature Contest” Iran 2015, Artist Unknown

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