Triglycerides are the form of fat used for long-term energy storage in your body. Poor health habits can lead to the elevation of levels of triglycerides in your blood, increasing your risk for blood clots and cardiovascular disease. Consumption of simple sugars and refined carbohydrates are the single biggest contributor to high triglyceride levels, according to the Cleveland Clinic.
Triglycerides are the form of fat most commonly found in food and in small amounts in the blood. A triglyceride molecule is constructed from three free fatty acids linked together to a backbone in the shape of an uppercase E. Where free fatty acids are intended for immediate energy production, triglycerides are used for long-term storage of fat energy due to their chemical stability.
Triglycerides, like cholesterol, are not soluble in water and must be linked to proteins to be carried through the blood. These proteins are called lipoproteins and can contribute to the buildup of plaque in your blood vessels. A poor diet and sedentary lifestyle typically leads to a high level of all lipids in your blood, medically called hyperlipidemia. However, it is possible for your triglycerides to be high without your blood pressure or cholesterol being high.
Role of Carbs
All carbohydrates are broken down into simple sugars to be absorbed into your body. Some carbs are broken into sugars rapidly, others slowly. In general, the more processed a carb is, the faster it is digested. As blood sugar rises after a meal, your body releases the hormone insulin to indicate to your cells it’s time to replenish their energy stores from the abundance of nutrients in the blood. However, if energy is not used due to low activity or the level of sugars in the blood is persistently high, the excess must be dealt with. Although some may be removed via urine and solid waste, the majority is converted into triglycerides for storage as fat. The increased production of triglycerides coupled with the resistance of fat from accumulating too rapidly leads to a buildup of triglycerides in the blood.
There are many ways to reduce the level of simple carbs in your diet. Primarily, avoid sweets and junk food. Substitute whole-grain products, avoiding highly refined flours and grains. Limit sweet beverages, such as soda and fruit juice, and alcohol. Choose vegetables, beans, legumes, whole grains and fruit as the majority of your carb sources. If you intend to eliminate substantial amounts of carbs from your diet, consult with your physician before beginning for guidance and advice tailored to your individual health.
Other Ways to Lower Triglycerides
Integrate regular physical activity into your life. If you are out of shape, small changes such as parking farther away or taking the stairs can make a difference. Eat foods rich in omega-3 fatty acids, such as cold-water fish, soybeans, flaxseed and walnuts. It may help to reduce overall calories and embark on a committed weight loss plan if you are overweight.
Sailors, most famously on arctic journeys found that a lack of fresh food led to them getting scurvy, a condition caused by lack of vitamin C,(ascorbic acid). A Scottish surgeon in the Royal Navy, James Lind, is accredited for solving this by taking on board limes or other Citrus fruits.
Lesser known is what Arctic Explorer, Vilhjalmur Stefansson learned from living with the native Inuit. Afflicted sailors who were able to abstain from other food and eat fresh meat (hunted on the ice-pack), were able to quickly recover from the condition. This is because, unlike humans, many mammals retain the ability to make their own ascorbic acid internally, and we can access this by eating them.
It would take them from 3 days to about 3 weeks to adapt to this high fat diet, then they thrived on it, despite the harsh working conditions.
Why Vitamin C is critical for the healthy function our immune systems
A Macrophage is a soldier of the immune system, that like Pac-Man gobbles up anything that is either a threat or no longer functional.
Much of what it eats is oxidative (thieves electrons from healthy tissues), so it must be packed with ascorbic acid (Vit C) which has an extra electron available to neutralize the cargo.
Glucose molecules have a similar chemical structure to ascorbic acid,(glucose has 4 extra hydrogen atoms) and so block or pre-saturate our brave macrophages.
These unarmed soldiers quickly become part of the oxidized goop that runs out your nose, or worse gets locked up in inflammation or arterial plaques
This is why attaining Vit. C will not help in a high glucose (carbohydrates) environment or in a situation where oxidative stress is overwhelming (such as from ingesting the oils from seeds high in omega 6).
Fresh fatty meat does contain enough vitamin C for our needs,(without the glucose hit) so long as we avoid excessive oxidative stress and glucose, (carbohydrates).
I avoid oxidative stress, so that the Vit C i am getting from precious fat animals is not wasted. Ascorbic acid will not even make it into my macrophages if they are pre-saturated in glucose. It’s a systemic perspective, that I find beautiful and simple, I try not to fight nature.
** “If an observer were watching for the onset of scurvy and had in mind, among other things, the psychiatric aspect, the first symptom noticed would probably be an emotional or temperamental change—the victim becomes more argumentative, more irritable, likelier to take affront, more inclined to pessimistic interpretations.** quote from the book The Fat of the Land
Also for a more accurate, (medical grade) explanation than this post and deeper look into the fascinating history, I totally recommend Amber L Hearn’s work
Facebook groups The carnivore way of eating has proved to be of enourmous benefit to people who have tried every thing else to heal disease and relieve chronic pain. Now it is being adopted by performance athletes, bio hackers and anybody looking to enjoy greater physical and mental health.
In the past three decades, total fat and saturated fat intake as a percentage of total calories has continuously decreased in Western diets, while the intake of omega-6 fatty acid increased and the omega-3 fatty acid decreased, resulting in a large increase in the omega-6/omega-3 ratio from 1:1 during evolution to 20:1 today or even higher. This change in the composition of fatty acids parallels a significant increase in the prevalence of overweight and obesity. Experimental studies have suggested that omega-6 and omega-3 fatty acids elicit divergent effects on body fat gain through mechanisms of adipogenesis, browning of adipose tissue, lipid homeostasis, brain-gut-adipose tissue axis, and most importantly systemic inflammation. Prospective studies clearly show an increase in the risk of obesity as the level of omega-6 fatty acids and the omega-6/omega-3 ratio increase in red blood cell (RBC) membrane phospholipids, whereas high omega-3 RBC membrane phospholipids decrease the risk of obesity. Recent studies in humans show that in addition to absolute amounts of omega-6 and omega-3 fatty acid intake, the omega-6/omega-3 ratio plays an important role in increasing the development of obesity via both AA eicosanoid metabolites and hyperactivity of the cannabinoid system, which can be reversed with increased intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). A balanced omega-6/omega-3 ratio is important for health and in the prevention and management of obesity.
Obesity is a complex condition involving the dysregulation of several organ systems and molecular pathways, including adipose tissue, liver, pancreas, gastrointestinal tract, the microbiome, the central nervous system (CNS), and genetics. The role of the CNS in obesity is receiving more attention as obesity rates rise and treatments continue to fail. While the role of the hypothalamus in the regulation of appetite and food intake has long been recognized, the roles of the CNS reward systems are beginning to be examined as the role of environmental influences on energy balance are explored. Furthermore, omega-3 fatty acids hold great promise in the prevention and management of obesity.
Omega-6 and omega-3 polyunsaturated fatty acids (PUFAs) are essential fatty acids that must be derived from the diet, cannot be made by humans, and other mammals because of the lack of endogenous enzymes for omega-3 desaturation [1,2]. Due to agribusiness and modern agriculture western diets contain excessive levels of omega-6 PUFAs but very low levels of omega-3 PUFAs, leading to an unhealthy omega-6/omega-3 ratio of 20:1, instead of 1:1 that was during evolution in humans (Figure 1) [1,3].
Eicosanoid products derived from omega-6 PUFAs (such as prostaglandin (PG) E2 and leukotriene (LT) B4 synthesized from arachidonic acid (AA)) are more potent mediators of thrombosis and inflammation than similar products derived from omega-3 PUFAs (PGE3 and LTB5 synthesized from eicosapentaenoic acid (EPA)) (Figure 2) (Table 1) [1,2,3].
Effects of Ingestion of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from Fish or Fish Oil. Modified from .
− Decreased production of prostaglandin E2 (PGE2) metabolites
− A decrease in thromboxane A2, a potent platelet aggregator and vasoconstrictor
− A decrease in leukotriene B4 formation, an inducer of inflammation, and a powerful inducer of leukocyte chemotaxis and adherence
− An increase in thromboxane A3, a weak platelet aggregator and weak vasoconstrictor
− An increase in prostacyclin PGI3
− Both PGI2 and PGI3 are active vasodilators and inhibitors of platelet aggregation
− An increase in leukotriene B5, a weak inducer of inflammation and a weak chemotactic agent
Thus, an unbalanced omega-6/omega-3 ratio in favor of omega-6 PUFAs is highly prothrombotic and proinflammatory, which contributes to the prevalence of atherosclerosis, obesity, and diabetes [1,2,3,4,5,6]. In fact, regular consumption of diets rich in omega-3 PUFAs have been associated with low incidence of these diseases, particularly in Icelandic populations, Inuit indigenous people, and Native Americans in Alaska [7,8,9]. However, using fish oil as the primary source of omega-3 PUFAs to treat type 2 diabetes has not always met with success [6,10,11]. Although nutritional studies suggest that high omega-6/omega-3 ratios have contributed significantly to the “obesity epidemic” [12,13], clinical trials using omega-3 PUFAs as weight-reducing agents have produced conflicting findings of both positive [14,15,16] and negative effects [17,18,19] due to many factors (Table 2).
Factors that affect outcomes in Obesity studies leading to conflicting results in clinical intervention trials (Modified from Reference ).
- Determination of the composition of the background diet in terms of omega-6 and omega-3 fatty acids and inflammatory markers i.e., US, UK and Northern European countries have the highest amount of LA + AA in their diets, which competes with omega-3 PUFAs; they also have the lowest amount of vegetable and fruit intake, which are needed for optimal absorption of omega-3 PUFA from supplements
- Background inflammation
- Some studies are using fish and others omega-3 supplements; studies show that a continuous daily intake of omega-3 supplements leads to higher concentrations in the blood than eating fish two times/week
- Variation in the dose of omega-3 fatty acids
- Variation in the number of subjects
- Variation in the severity of disease
- Variation in the pharmacologic treatment
- Genetic variants predisposing to Obesity
- Dietary intake by means of questionnaires instead of actual measurements of omega-3 PUFAs in the red blood cell membrane phospholipids or plasma is a major problem that leads to conflicting results
- Length of intervention
- Genetic variants in the metabolism of omega-6 and omega-3 fatty acids
This paper focuses, on the differential aspects of omega-6 and omega-3 fatty acids and their ratio, in energy balance and in the prevention and management of obesity.
2. The Importance of the Omega-6/Omega-3 Fatty Acid Ratio: Metabolic, Physiological and Evolutionary Aspects
There are two classes of essential fatty acids (EFA), omega-6 and omega-3. The distinction between omega-6 and omega-3 fatty acids is based on the location of the first double bond, counting from the methyl end of the fatty acid molecule. Omega-6 fatty acids are represented by linoleic acid (LA) (18:2ω-6) and omega-3 fatty acids by alpha-linolenic acid (ALA) (18:3ω-3). LA is plentiful in nature and is found in the seeds of most plants except for coconut, cocoa, and palm. ALA, on the other hand, is found in the chloroplasts of green leafy vegetables, and in the seeds of flax, rape, chia, perilla and walnuts. Both essential fatty acids are metabolized to longer-chain fatty acids of 20 and 22 carbon atoms. LA is metabolized to arachidonic acid (AA) (20:4ω6) while ALA is metabolized to eicosapentaenoic acid (EPA) (20:5ω3) and docosahexaenoic acid (DHA) (22:6ω3). This is achieved by increasing the chain length and the degree of unsaturation by adding extra double bonds to the carboxyl end of the fatty acid molecule  (Figure 3). AA is found predominantly in the phospholipids of grain-fed animals, dairy and eggs. EPA and DHA are found in the oils of fish, particularly fatty fish.
In mammals, including humans, the cerebral cortex, retina, testis and sperm are particularly rich in DHA. DHA is one of the most abundant components of the brain’s structural lipids. DHA, like EPA, can be derived only from direct ingestion or by synthesis from dietary EPA or ALA: humans and other mammals, except for certain carnivores such as lions, can convert LA to AA and ALA to EPA and DHA, although the process is slow [21,22]. There is competition between omega-6 and omega-3 fatty acids for the desaturation enzymes. Both fatty acid desaturase 1 (FADS1) and fatty acid desaturase 2 (FADS2) prefer ALA to LA [21,23,24]. However a high LA intake, such as that characterizing Western diets, interferes with the desaturation and elongation of ALA [22,23,24,25]. Similarly, trans fatty acids interfere with the desaturation and elongation of both LA and ALA.
There are important genetic variables in fatty acid biosynthesis involving FADS1 and FADS2, which encode rate-limiting enzymes for fatty acid metabolism (Figure 3). Ameur et al.  performed genome-wide genotyping (n = 5652 individuals) of the FADS region in five European population cohorts and analyzed available genomic data from human populations, archaic hominins, and more distant primates. Their results show that present-day humans have two common FADS haplotypes A and D that differ dramatically in their ability to generate long-chain polyunsaturated fatty acids (LC-PUFAs). The most common haplotype, denoted haplotype D, was associated with high blood lipid levels (p = 1 × 10−65), whereas the less common haplotype (haplotype A) was associated with low blood lipid levels (p = 1 × 10−52). The haplotype D associated with the enhanced ability to produce AA and EPA from their precursors LA and ALA respectively is specific to humans and has appeared after the split of the common ancestor of humans and Neanderthals. This haplotype shows evidence of a positive selection in African populations in which it is presently almost fixed and it is less frequent outside of Africa. Haplotype D provides a more efficient synthesis of LC-PUFAs and in today’s high LA omega-6 dietary intake from vegetable oils, it leads to increased synthesis of AA from LA. As a result Haplotype D represents a risk factor for coronary heart disease (CHD), cancer, obesity, diabetes and the metabolic syndrome, adding further to health disparities in populations of African origin living in the West, in addition to lower socioeconomic status [27,28]. Furthermore, FADS2 is the limiting enzyme and there is some evidence that it decreases with age . Premature infants , hypertensive individuals , and some diabetics  are limited in their ability to make EPA and DHA from ALA. These findings are important and need to be considered when making dietary recommendations. Genetic variants in FADS cluster are determinants of long-chain PUFA levels in circulation, cells and tissues. These genetic variants have been studied in terms of ancestry, and the evidence is robust relative to ethnicity. Thus, 80% of African Americans and about 45% of European Americans carry two copies of the alleles associated with increased levels of AA. It is quite probable that gene PUFA interactions induced by the modern Western diet are differentially driving the risk of diseases of inflammation (obesity, diabetes, atherosclerosis and cancer) in diverse populations.
As mentioned earlier, mammalian cells cannot convert omega-6 to omega-3 fatty acids because they lack the converting enzyme, omega-3 desaturase. Omega-6 and omega-3 fatty acids are not interconvertible, are metabolically and functionally distinct, and often have important opposing physiological effects, therefore their balance in the diet is important. When humans ingest fish or fish oil, the EPA and DHA from the diet partially replace the omega-6 fatty acids, especially AA, in the membranes of probably all cells, but especially in the membranes of platelets, erythrocytes, neutrophils, monocytes, and liver cells (reviewed in [3,32]). AA and EPA are the parent compounds for eicosanoid production. Because of the increased amounts of omega-6 in the Western diet, the eicosanoid metabolic products from AA, specifically prostaglandins, thromboxanes, leukotrienes, hydroxy fatty acids, and lipoxins, are formed in larger quantities than those derived from omega-3 fatty acids, specifically EPA . The eicosanoids from AA are biologically active in very small quantities and, if they are formed in large amounts, they contribute to the formation of thrombus and atheromas; to allergic and inflammatory disorders, particularly in susceptible people; and to proliferation of cells . Thus, a diet rich in omega-6 fatty acids shifts the physiological state to one that is proinflammatory, prothrombotic, and proaggregatory, with increases in blood viscosity, vasospasm, vasoconstriction and cell proliferation.
A balance existed between omega-6 and omega-3 fatty acids during the long evolutionary history of the genus Homo . During evolution, omega-3 fatty acids were found in all foods consumed: particularly meat, fish, wild plants, nuts and berries [34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50]. Recent studies by Cordain et al.  on the composition of the meat of wild animals confirm the original observations of Crawford and Sinclair et al. [36,52]. However, rapid dietary changes over short periods of time as have occurred over the past 100–150 years is a totally new phenomenon in human evolution (Figure 1). A balance between the omega-6 and omega-3 fatty acids is a physiological state that is less inflammatory in terms of gene expression , prostaglandin and leukotriene metabolism, and interleukin-1 (IL-1) production .
Modern agriculture, by changing animal feeds as a result of its emphasis on production, has decreased the omega-3 fatty acid content in many foods: animal meats, eggs, and even fish [39,40,41,42]. Foods from edible wild plants contain a good balance of omega-6 and omega-3 fatty acids. Purslane, a wild plant, in comparison to spinach, red leaf lettuce, buttercrunch lettuce and mustard greens, has eight times more ALA than the cultivated plants . Modern aquaculture produces fish that contain less omega-3 fatty acids than do fish grown naturally in the ocean, rivers and lakes . The fatty acid composition of egg yolk from free-ranging chicken has an omega-6:omega-3 ratio of 1.3 whereas the United States Department of Agriculture (USDA) egg has a ratio of 19.9 . By enriching the chicken feed with fishmeal or flaxseed, the ratio of omega-6:omega-3 decreased to 6.6 and 1.6 respectively.
Although diets differ in the various geographic areas , a number of investigators including Crawford , Cordain , Eaton  and Kupiers  have shown that during the Paleolithic period, the diets of humans included equal amounts of omega-6 and omega-3 fatty acids from both plants (LA + ALA) and from the fat of animals in the wild and fish (AA + EPA + DHA). Recent studies by Kuipers et al.  estimated macronutrient and fatty acid intakes from an East African Paleolithic diet in order to reconstruct multiple Paleolithic diets and thus estimate the ranges of nutrient intakes on which humans evolved. They found (range of medians in energy %) intakes of moderate-to-high protein (25%–29%), moderate-to-high fat (30%–39%) and moderate carbohydrates (39%–40%). Just as others have concluded previously, Kuipers et al.  stated, “compared with Western diets, Paleolithic diets contained consistently high protein and long-chain PUFA and lower LA”. Guil-Guerrero J et al.  determined the fat composition of frozen mammoths (from 41,000 to 34,000 years BP), Bisons from early Holocene (8200–9300 years BP) and horses from middle Holocene (4600–4400 years BP), often consumed by Paleolithic/Neolithic hunters gatherers, and concluded, that “the animal fat contained suitable amounts of omega-3 and omega-6 fatty acids, possibly in quantities sufficient to meet today’s dietary requirements for good health”. The elucidation of sources of omega-3 fatty acids available for the humans who lived in the Paleolithic and Neolithic is highly relevant to ascertain the availability of nutrients at that time and to draw conclusions about healthy dietary habits for present-day humans. As in previous studies, the amount of ALA was higher than LA in the fat of the frozen specimens [58,59] (Table 3 and Table 4).
Estimated Omega-3 and Omega-6 Fatty Acid intake in the Late Paleolithic Period (g/day) a,b,c.
Ratios of ω6/ω3
AA + DTA/EPA + DPA + DHA
a Data from Eaton et al. ; b Assuming an energy intake of 35:65 of animal: plant sources; c LA, linoleic acid; ALA, linolenic acid; AA, arachidonic acid; EPA, eicosapentaenoic acid; DTA, docosatetranoic acid; DPA, docosapentaenoic acid; DHA, docosahexaenoic acid.
Omega-6/Omega-3 Ratios in Different Populations.
Greece prior to 1960
Current India, rural
Current UK and northern Europe
Current India, urban
3. Effects of Omega-6 and Omega-3 Fatty Acids and their Ratio on Obesity
Experimental studies have suggested that omega-3 and omega-6 fatty acids may elicit divergent effects on body fat gain through mechanisms of adipogenesis , lipid homeostasis [61,62], brain-gut-adipose tissue axis , and systemic inflammation . Metabolites of AA (20:4ω-6) play important roles in the terminal differentiation of pre-adipocyte to mature adipocyte . This effect can be inhibited by omega-3 fatty acids at multiple steps [66,67,68,69]. Omega-6 fatty acids increase cellular triglyceride content by increasing membrane permeability , while omega-3 fatty acids reduce fat deposition in adipose tissues by suppressing lipogenic enzymes and increasing β-oxidation . In addition, omega-6 and omega-3 fatty acids differentially modulate the brain-gut-adipose tissue axis  and the inflammatory properties of downstream eicosanoids, which ultimately affect pre-adipocyte differentiation and fat mass growth . White adipocytes are storing energy in the form of triglycerides whereas brown adipocytes dissipate energy from triglycerides by producing heat (Table 5). In rodents and possibly in humans both types of fat cells participate in the total energy balance. By altering rates of adipocyte differentiation and proliferation, differences in fatty acid composition of dietary fats may also contribute to adipose tissue development, in particular with respect to the relative intake of omega-6 and omega-3 fatty acids. The omega-6/omega-3 ratio determines the availability of omega-6-AA within adipose tissue and thus the level of various prostaglandins derived from the cyclooxygenase-mediated pathways, which can be blocked by omega-3 fatty acids (Figure 2). Recent studies have shown that perinatal exposure of mice to a high omega-6 fatty acid diet (similar to Western diet) results in a progressive accumulation of body fat across generations, which is consistent with the fact that in humans, overweight and obesity have steadily increased in the last decades, and emerge earlier in life [12,73]. Furthermore, AA metabolites prostaglandins E2 and F2α have an inhibitory role in the browning process of white fat cells converted into energy-dissipating brown fat cells which are believed to play a role in controlling energy balance by lowering body weight [74,75,76,77,78,79,80,81,82] (Table 5).
Opposing Effects of Omega-6 and Omega-3 Fatty Acids in Obesity.
High AA via the PI2 receptor activates the cAMP protein kinase A, signaling pathway leads to proliferation and differentiation of WAT, prevention of its browning through inhibition of PPARy target genes including UCPI, decrease mitochondrial biogenesis , increasing triglycerides , insulin resistance, leptin resistance, decreased adiponectin levels, decreased fatty acid oxidation and hepatic steatosis .
High EPA and DHA partially inhibit cAMP signaling pathways triggered by AA at levels upstream of PKA  block COX-2 metabolites PGI2 and PGEF2a that stimulate white adipogenesis and inhibit the browning process respectively, prevent increased triglycerides and adipose tissue proliferation through UCP-I and PPARy activation, increased mitochondrial biogenesis, increased fatty acid oxidation, and apoptosis [71,75].
AA metabolites prostaglandin 2 thromboxane 2 and leukotriene 4 are prothrombotic and proinflammatory leading to increased production of IL-1, IL-6, NFKB and TNF and inflammation [1,64].
High dietary intake of EPA and DHA blocks the metabolites of AA and prevents inflammation, which is the hallmark of obesity [1,64,67].
Insulin Resistance Leptin Resistance Adiponectin
AA leads to insulin resistance, leptin resistance, lower adiponectin and hepatic steatosis. AA blunts PI3-Akt pathway leading to leptin resistance in the brain and deregulation of food intake [19,76,77].
EPA and DHA regulate glucose utilization, insulin sensitivity (Akt phosphorylation) in part mediated by PPARy and AMPK activation . EPA and DHA regulate the secretion of adipokines involved in energy homeostasis and intermediate metabolism and in glucose and lipid metabolism. DHA restores insulin sensitivity in skeletal muscle by preventing lipotoxicity and inflammation [78,79].
AA increases the concentration of (2-AG) and (AEA) leading to excessive endocannabinoid signaling, and dysregulation of the cannabinoid system, weight gain, larger adipocytes and more macrophages in adipose tissue , inflammation and a metabolic profile associated with obesity [81,82].
EPA and DHA decrease 2-AG and AA in the brain while increasing DHA, decreasing the dysregulation of the cannabinoid system, improving insulin sensitivity and decreasing central body fat.
High intake of omega-6 fatty acids during the perinatal period is associated with increased adiposity in the offspring. In human studies the level of AA in adipose tissue is associated with the BMI and overweight status of children. High omega-6/omega-3 fatty acids in umbilical cord red blood cell (RBC) membrane phospholipids was associated with high subscapular skin-fold thickness at 3 years of age .
Animal and human studies have shown that EPA and DHA supplementation may be protective against obesity, and may reduce weight gain in already obese animals and humans . Specifically, studies demonstrated a reduction in visceral (epididymal and/or retroperitoneal) fat in rats fed high lipid diets that incorporate omega-3 PUFAs [75,78,79,84,85,86,87], and the effect was dose-dependent . The reduction in visceral fat was associated with a decrease in adipocyte size [85,86] and number . High fat diets rich in omega-6 fatty acids have been shown to increase the risk of leptin resistance, diabetes, and obesity in humans and rodents [76,88]. AA impairs hypothalamic leptin signaling and energy homeostasis in mice . The inhibitory role of AA has been suggested in both basal and insulin-stimulated leptin expression and production .
3.1. The Fat-1 Transgenic Mouse Model
Many of the problems involving dietary animal studies can be overcome by the fat-1 transgenic mouse model that carries a Caenorhabditis elegans fat-1 gene encoding an omega-3 fatty acid desaturase. This enzyme can convert omega-6 to omega-3 fatty acids by adding a double bond at the omega-3 position . Consequently, fat-1 not only increases the levels of omega-3 fatty acids but also concomitantly decreases omega-6 fatty acids as well as the omega-6/omega-3 ratio—a goal difficult to achieve through dietary means alone, yet important for health benefits. Although not fully equated to a dietary approach, the transgenic model produces the same types of omega-3 fatty acids as those obtained through diet .
Furthermore, the fat-1 model offers numerous advantages in the studies of the health benefits of omega-3 fatty acids, because the transgenic model allows elucidation of the mechanisms of actions of omega-3 fatty acids without the confounding issues associated with dietary approaches, such as dose, composition, and duration of treatment applied in different studies [16,90,91] (Table 2). The use of fat-1 mouse model avoids these concerns by feeding exactly the same diet to the transgenic and wild type (WT) mice. Because FAT-1 is an enzyme, the production of omega-3 fatty acids in mice is limited by the amount of available substrate: omega-6 fatty acids. The degree of increase in omega-3 fatty acids (3- to 4-fold) required to improve metabolic parameters in fat-1 transgenic mice has been shown to be achievable through dietary means in animals and humans . Recently Li et al.  carried out a comprehensive study using the fat-1 model to better define how alterations in the tissue levels of omega-6 and omega-3 fatty acids affect energy balance, lipid and glucose metabolism, chronic inflammation, and the underlying molecular events (or mechanisms). Their results show that when challenged with high-fat diets, fat-1 mice strongly resisted obesity, diabetes, hypercholesterolemia, and hepatic steatosis. Endogenous elevation of omega-3 PUFAs and reduction of omega-6 PUFAs did not alter the amount of food intake but led to increased energy expenditure in the fat-1 mice. These metabolic phenotypes were accompanied by attenuation of the inflammatory state because tissue levels of prostaglandin E2, leukotriene B4, monocyte chemoattractant protein-1, and TNF-α were significantly decreased. The TNF-α-induced NF-κB signaling was almost completely abolished. Consistent with the reduction in chronic inflammation and a significant increase in peroxisome proliferator-activated receptor-γ activity in the fat-1 liver tissue, hepatic insulin signaling was sharply elevated. The activities of prolipogenic regulators, such as liver X receptor, stearoylCoA desaturase-1, and sterol regulatory element binding protein-1 were sharply decreased, whereas the activity of peroxisome proliferator-activated receptor-α, a nuclear receptor that facilitates lipid β-oxidation, was markedly increased . Thus, endogenous conversion of omega-6 to omega-3 PUFAs via fat-1 strongly protects against obesity, diabetes, inflammation, and dyslipidemia and may represent a novel therapeutic modality to treat these prevalent disorders.
3.2. Human Studies
Randomized controlled trials in humans examining the relationship between omega-3 supplementation and body composition have produced conflicting results due to many factors summarized in Table 2 [19,83]. This may be due to differences in study design, dosage, not taking into consideration the omega-6/omega-3 ratio of the background diet, timing, and duration of omega-3 PUFA administration, use of other supplements in addition to omega-3 PUFA, and demographics of the study population. Furthermore, in many studies the determination of omega-6/omega-3 fatty acids was based on food frequency questionnaires, which are not as accurate as direct measurements of fatty acids in RBC membrane phospholipids. Several studies have provided supporting evidence for a role of omega-3 PUFAs in body composition , weight reduction , less hunger and more fullness . These findings support a potential role for omega-3 in appetite regulation in humans. Some intervention studies showed that omega-3 fatty acid supplementation reduced body weight and obesity in lean , overweight [95,97] and obese  individuals. Couet et al.  noted a 22% increase in basal lipid oxidation with 6 grams of fish oil for 3 weeks. Omega-3 fatty acids are long term metabolic fuel partitioners with greater partitioning towards β-oxidation in men than in women.
Omega-6 and omega-3 red blood cell membrane phospholipid determinations represent biomarkers of dietary intake plus endogenous metabolism and represent the most accurate way to carry out preventive studies and clinical intervention studies to evaluate their role in weight gain and obesity . Wang et al. conducted a prospective analysis to examine the association of baseline red blood cell membrane phospholipids of omega-3 fatty acids, omega-6 fatty acids, omega-6/omega-3 ratio and trans fatty acids with the longitudinal changes in body weight and the risk of becoming overweight or obese during a mean of 10.4 years follow up in the NIH Women’s Health Initiative Study. The results of this prospective study showed that baseline red blood cell membrane phospholipids cis omega-3 fatty acids is inversely associated, and cis omega-6 fatty acids are positively associated, with longitudinal weight gain in initially normal weight healthy women. This is the first study to prospectively examine omega-3 and omega-6 fatty acids in red blood cell membrane phospholipids in relation to weight gain and the risk of becoming overweight or obese. After multivariable adjustment, significant positive associations with weight gain were found only for dihomo-γ-linolenic acid (DGLA), LA, and Gamma-linolenic acid (GLA) among omega-6 fatty acids and trans 18:1 among trans fatty acids; while inverse associations were found with EPA among omega-3 fatty acids. The authors state that, “the variations by individual fatty acids may be due to unknown and uncontrolled factors involved in the conversion and metabolism of each fatty acid, and should be interpreted cautiously given the multiple comparisons. This study included only women who had normal BMI at baseline to minimize potential confounding and address the risk of becoming overweight or obese”. To further evaluate the impact of baseline BMI on the results, Wang et al.  stratified analyses by baseline BMI levels (18.5–≤23, 23–≤25 kg/m2) and also included women who were already overweight or obese at baseline (baseline BMI ≥ 25 kg/m2) in sensitivity analyses. Similar patterns of associations were found in these additional analyses. In conclusion, this prospective study provided strong suggestive evidence that omega-3 fatty acids in RBC membrane phospholipids are inversely associated, while cis omega-6 fatty acids, omega-6/omega-3 ratio, and trans fatty acids are positively associated, with longitudinal weight gain.
4. Genetics: The Fat Mass and Obesity-Associated Gene
Genome-Wide Association Studies (GWAS) have identified more than 90 loci that contain genetic variants associated with obesity. Many of these variants are in intronic regions. The strongest genetic association with risk to polygenic obesity are single-nucleotide variants (SNV) in intron 1 and 2 of the FTO (fat mass and obesity associated) gene. There are 89 SNVs in FTO intron 1 and 2. Deciphering how these variants regulate gene expression has been difficult. Recently Claussnitzer et al.  reported a strategy and defined the causal SNV and the mechanisms of function in preadipocytes. The authors provide evidence for the rs 1421085 T to C SNV to result in a cellular phenotype consistent with obesity in primary human adipocytes, including decreased mitochondrial energy generation and increased triglyceride accumulation.
Their study provided evidence that the risk allele rs 1411085 T to C SNV resulted in increased expression of IRX3 and IRX5 genes in pre-adipocytes, which shifted the development of these cells toward the “white program” and increased lipid storage, whereas knockdown of IRX3 and IRX5 genes restored thermogenesis in adipocytes from persons at high risk for obesity. Thus, the risk allele functioned similarly to AA metabolites, PGI2 and PGF2a, increasing proliferation of white adipose tissue and decreasing its browning respectively, whereas the knockdown of IRX3 and IRX5 genes functioned similarly to omega-3 fatty acid metabolites increasing the browning of the adipose tissue, mitochondrial biogenesis and thermogenesis. The arachidonic acid metabolites PGI2 and PGF2a lead to increases in white adipose tissue and decreases its browning respectively. Human studies have shown a direct relationship between plasma arachidonic acid levels and infant body weight, as well as between AA levels in adipose tissue lipids and BMI in children in Cyprus and Crete [102,103]. AA directly inhibits UCPI gene expression. Considering the high omega-6/omega-3 fatty acid ratio of Western diets and the role of AA in adipose cell differentiation, proliferation, and decreasing browning of white adipose tissue, further research should include studies on the effects of omega-3 fatty acids in blocking the effects of the risk allele (rs 1421085), which appears to be responsible for the association between the first intron of FTO gene and obesity in humans.
5. Omega-6/Omega-3 Fatty Acid Ratio: Endocannabinoid System
A diet high in the omega-6/omega-3 ratio causes an increase in the endocannabinoid signaling and related mediators, which lead to an increased inflammatory state, energy homeostasis, and mood. In animal experiments a high omega-6 acid intake leads to decreased insulin sensitivity in muscle and promotes fat accumulation in adipose tissue. Nutritional approaches with dietary omega-3 fatty acids reverse the dysregulation of this system, improve insulin sensitivity and control body fat.
Endocannabinoids are lipids, derived from the omega-6 AA. Their concentrations are regulated by (1) dietary intake of omega-6 and omega-3 fatty acids; and (2) by the activity of biosynthetic and catabolic enzymes involved in the endocannabinoid pathway, which is an important player in regulation of appetite and metabolism [81,104]. The endocannabinoid system is involved in regulation of energy balance and sustained hyperactivity of the endocannabinoid system contributes to obesity [81,82]. AA is the precursor of 2-arachidonoylglycerol (2-AG) and anandamide (AEA). Increasing the precursor pool of AA causes excessive endocannabinoid signaling leading to weight gain and a metabolic profile associated with obesity. Endocannabinoids activate endogenous cannabinoid CB1 and CB2 receptors in the brain, liver, adipose tissue, and the gastrointestinal tract . Activation of CB1 receptors in the hypothalamus leads to increased appetite and food intake . In mouse experiments endocannabinoids selectively enhance sweet taste, which in the current highly palatable food supply stimulate food intake . The endocannabinoid system functions in concert with other systems regulating food intake and energy balance, and is regulated by leptin, insulin, ghrelin, cholecystokinin, and other signals. Targeting the endocannabinoid system has been a strategy for weight loss. Randomized controlled clinical trials in overweight or obese humans showed that CB1 receptor antagonists such as rimonabant led to significant weight loss after one year of treatment . However the drug was withdrawn from the market due to severe side effects that led to increased risk of anxiety, depression, and suicide .
Alvheim et al.  carried out an experiment in mice at six weeks of age, in which increasing the linoleic acid in the diet led to increases in AA in red blood cell membrane phospholipids, elevated 2-AG and AEA in liver, elevated plasma-leptin and resulted in larger adipocytes and more macrophage infiltration in adipose tissue. It was also noted that a higher linoleic acid increased feed efficacy and caused greater weight gain than isocaloric diets containing less LA. Increasing the dietary LA from 1% to 8% of energy increased liver endocannabinoid levels, which increased the risk of developing obesity, even in a low fat diet. Mice chronically deficient in omega-3 PUFA have significantly lower concentrations of DHA in brain phospholipids, and higher 2-AG (derived from AA) compared to mice with sufficient omega-3 PUFA in their diet . Furthermore, omega-3 PUFA supplementation of mice with 10% weight DHA-rich fish oil for 4 weeks led to higher brain DHA levels compared to mice on a low omega-3 PUFA diet, and led to a significant decrease in brain 2-AG and brain AA. This nutritional approach with dietary omega-3 PUFA, reversed the dysregulation of the cannabinoid system, improved insulin sensitivity and decreased central body fat.
6. Conclusions and Recommendations
Human beings evolved on a diet that was balanced in the omega-6 and omega-3 essential fatty acids.
A high omega-6 fatty acid intake and a high omega-6/omega-3 ratio are associated with weight gain in both animal and human studies, whereas a high omega-3 fatty acid intake decreases the risk for weight gain. Lowering the LA/ALA ratio in animals prevents overweight and obesity.
Omega-6/omega-3 fatty acids compete for their biosynthetic enzymes and because they have distinct physiological and metabolic properties, their balanced omega-6/omega-3 ratio is a critical factor for health throughout the life cycle.
Adipose tissue is the main peripheral target organ handling fatty acids, and AA is required for adipocyte differentiation (adipogenesis). The increased LA and AA content of foods has been accompanied by a significant increase in the AA/EPA + DHA ratio within adipose tissue, leading to increased production in AA metabolites, PGI2 which stimulates white adipogenesis and PGF2α which inhibits the browning process, whereas increased consumption of EPA and DHA leads to adipose tissue homeostasis through adipose tissue loss and increased mitochondrial biogenesis.
High omega-6 fatty acid intake leads to hyperactivity of endocannabinoid system, whereas omega-3 fatty acids lead to normal homeostasis (decrease hyperactivity).
High omega-6 fatty acids increase leptin resistance and insulin resistance, whereas omega-3 fatty acids lead to homeostasis and weight loss.
Because a high omega-6/omega-3 ratio is associated with overweight/obesity, whereas a balanced ratio decreases obesity and weight gain, it is essential that every effort is made to decrease the omega-6 fatty acids in the diet, while increasing the omega-3 fatty acid intake. This can be accomplished by (1) changing dietary vegetable oils high in omega-6 fatty acids (corn oil, sunflower, safflower, cottonseed, and soybean oils) to oils high in omega-3s (flax, perilla, chia, rapeseed), and high in monounsaturated oils such as olive oil, macadamia nut oil, hazelnut oil, or the new high monounsaturated sunflower oil; and (2) increasing fish intake to 2–3 times per week, while decreasing meat intake.
In clinical investigations and intervention trials it is essential that the background diet is precisely defined in terms of the omega-6 and omega-3 fatty acid content. Because the final concentrations of omega-6 and omega-3 fatty acids are determined by both dietary intake and endogenous metabolism, it is essential that in all clinical investigations and intervention trials the omega-6 and omega-3 fatty acids are precisely determined in the red blood cell membrane phospholipids. In severe obesity drugs and bariatric surgery have been part of treatment.
The risk allele rs 1421085 T to C SNV in intron 1 and 2 in the FTO gene functioned similarly to AA metabolites, PGI2 and PGF2a increasing proliferation of white adipose tissue and decreasing its browning respectively, whereas the knockdown of IRX3 and IRX5 genes functioned similarly to omega-3 fatty acid metabolites increasing the browning of white adipose tissue, mitochondrial biogenesis, and thermogenesis. Therefore, further research should include studies on the effects of omega-3 fatty acids in blocking the effects of the risk allele (rs 1421085), which appears to be responsible for the association between the first intron of FTO gene and obesity in humans.
In the future studies on genetic variants from GWAS will provide opportunities to precisely treat and prevent obesity by both nutritional and pharmaceutical interventions.
Obesity is a preventable disease that can be treated through proper diet and exercise. A balanced omega-6/omega-3 ratio 1–2/1 is one of the most important dietary factors in the prevention of obesity, along with physical activity. A lower omega-6/omega-3 ratio should be considered in the management of obesity.
I have not received any source of funding for this article.
Conflicts of Interest
The author declares no conflict of interest.
Source: Article by Artemis P. Simopoulos (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4808858/)
However, if you look at the backdrop before the heart health epidemic, you cannot ignore the rise of vegetable oils as a dietary staple. This was led by the efforts of Procter & Gamble and their new creation, Crisco, the first shortening to be made entirely of vegetable oil.
Starting in 1911, crisco was adeptly marketed by Procter & Gamble as a more versatile butter. It could be used for frying, baking and cooking. It could be stored at room temperature. They even claimed it was easier to digest and healthier too.
Vegetable oil consumption went from 11 pounds per person per year to 59.
Yet Ancel Keys and the AHA blamed the entire heart attack epidemic on butter, a food that was falling in consumption.
So here’s how the story goes:
Step 1: Get everybody to eat hydrogenated vegetable oils under the guise of health
Step 2: See massive heart disease increase
Step 3: Blame it on butter and natural fats, and tell people to eat MORE of the vegetable oils
Step 4: Pharma, doctors and CPG companies profit. The individual loses.
This sums up the last 100 years of health. Our genetic code has only changed ~0.005% over the last 40,000 years but our diets have changed over 1000x [*]
Because of Ancel Keys and the government’s dietary recommendations, these vegetable oils are now found everywhere.
Why Is Vegetable Oil Bad For You?
Before we get into the actual consequences, why are vegetable oils so damaging?
Fatty Acid Instability
There are three kinds of fatty acids:
Polyunsaturated fatty acids
Monounsaturated fatty acids
Saturated fatty acids
What delineates between the three are how many double bonds each has.
Polyunsaturated acids are naturally occuring.
Canola oil has a high poly and monounsaturated fatty acid content (the form of polyunsaturated fatty acid is linoleic acid).
This is different from butter, which is almost all saturated fat. But what makes them of interest is that because of the multiple double bonds, they’re highly unstable.
It’s why butter is a solid at room temperature and canola oil is not.
The double bonds allow oxygen to sneak in and oxidize the fatty acids, particularly when heated. When “oxidized” they produce free radicals. Free radicals are electrons that play a role in every known disease.
They are unpaired electrons looking to find a match. In the process of doing so, they restructure every single cell they come into contact with. Think of them like a drunk person in a single’s bar.
Cooking foods in vegetable oils blasts them with these free radicals, which can destroy every cell in your body. It also produces toxic by-products discussed below.
When broken down and oxidized, polyunsaturated fatty acids produce toxic byproducts. One type of polyunsaturated acid in particular, omega 6’s, produce the worst toxins.
The three best studied toxins are Acrolein, HNE and MDA. Acrolein is the toxin found in cigarette smoke that causes lung damage. It is a biocide, meaning it kills all life. HNE and MDA are both cytotoxic and mutagenic — they kill cells and alter DNA.
And worst of all is that these toxic byproducts are highly reactive, leading to a cascade of toxic byproduct production when they’re in your body. Think of them like reactive zombies that infect every other fatty acid.
Omega 3 : Omega 6 Ratio
You may have heard of omega 3 and omega 6s. These are polyunsaturated fatty acids. Omega 3s have their first double bond on the 3rd carbon and omega 6s have their first double bond on the 6th. They are both polyunsaturated fatty acids.
Vegetable oils, like canola oil, are predominantly omega 6 fatty acids, such as linoleic acid.
Omega 3s and omega 6s are critical structural components. They have conflicting physiological effects, so the ratio between the two in the diet is important.
As you replace omega 3s with omega 6s in your diet, your body rapidly converts your structural components into whichever you consume. This shows up directly in human fatty tissue. As a result, from 1960 to 1986, the linoleic acid content in human fat tripled from 6% to 18% [*].
If our body was a house, we’d be constructed with radioactive nuclear waste instead of sturdy concrete under this new paradigm.
Additionally, a diet high in the omega 6: omega 3 ratio shifts your body to a proinflammatory state. And inflammation has been implicated in every chronic disease.
People in the paleolithic world were eating an omega 6 : omega 3 ratio of less than one. But because of canola and vegetable oils, the ratio has increased to over 15x in modern times.
Pretty much every disease can be linked to this increase. [*]
There’s also evidence that omega 6 fatty acids inhibit the anti-inflammatory effects of omega 3s [*].
Diseases Directly Linked to Vegetable Oils
Vegetable oils via the mechanisms above are implicated in almost every disease.
Vegetable oils cause all of the following:
We are about to touch on a handful of them below.
Alzheimers and Cognitive Disorders
Vegetable oils are the worst thing for your brain. It’s like cutting your head open and putting an iron directly on its surface. Maybe even worse, because at least that would get out some of the wrinkles…
HNE, the toxic byproduct mentioned above, is always found in damaged areas of the brain. And injecting it directly into rodents has been shown to cause the amyloid plaques which are typical of Alzheimer’s disease [*].
In another study on mice, a diet high in canola oil was shown to significantly impair memory and lead to amyloid plaques [*].
Alzheimer’s disease is characterized by reduced synapse activity and energy impairment. One of the main causes is the buildup of these plaques. Another is from deficient energy generation. HNE has been shown to damage mitochondrial ATP generation [*] — the fuel needed for your brain.
Lastly, HNE has been shown to increase oxidative stress in the brain and destroy the nerve cell highways called microtubules [*].
Your brain is 60% fat and it’s composed of the fat that you consume. If you consume toxic, unstable, inflammatory fats, then that is what your brain will be made of. As the saying goes, “you are what you eat.”
Eating vegetable oils turns your brain into Chernobyl — a nuclear wasteland.
No wonder cognitive disorders are on the rise.
Cancer is caused by oxidative stress, mitochondrial dysfunction and genetic damage. Seed oils have been shown to cause all three.
Linoleic acid is even required in animal models to induce cancer. This study pictured below showed that tumors started once rats consumed 20% of fatty acids in the form of linoleic acid. Without the oxidative byproducts, cells reproduce normally and retain metabolic functionality [*].
One of the main mechanisms by which vegetable oils cause cancer is through cardiolipin damage. Cardiolipin is one of the main phospholipids in the mitochondria — the energy powerhouse of the cell.
When cardiolipin is damaged, this impairs the mitochondria’s metabolic efficiency, which is one of the hallmarks of cancer (the Warburg Effect) [*]. No tumor has ever been found with normal cardiolipin [*]. Ultimately, damaged cardiolipin causes a vicious cycle which damages metabolism and causes the production of even more toxic byproducts.
This theory has been propounded by Thomas Seyfried who deemed cancer a mitochondrial metabolic disease [*]. The connection to seed oils is profound given HNE and seed oils’ primary mechanism of damage is to the mitochondria’s metabolism.
HNE has also been shown to mutate mitochondrial DNA and cause oxidative damage. It also damages the p53 gene, which is a tumor suppressor [*]. Damage to this gene occurs in many cancers.
Once again, this is due to the mutagenic properties of seed oils and their unstable nature.
What’s clear is that the rise of all these cancers is not a fluke. It’s a direct corollary of the increase in vegetable oil consumption and the disastrous AHA recommendations.
And lastly, the gold standard of studies — a controlled study (instead of the epidemiological nonsense) showing that over an eight year period, a group of men treated with a diet high in vegetable oils had 2x the cancer rate [*].
It’s like the entire world is smoking packs of cigarettes, getting lung cancer and we’re encouraging them to do even more of it.
Diabetes is characterized by insulin resistance and high levels of blood sugar. It’s caused after pancreas’ beta cells no longer secrete adequate insulin to halt hepatic glucose production (the liver’s release of glucose).
Seed oils play a large causal role.
In this study below, mice were placed on a high fat diet [*]. One group consumed olive oil and the other consumed vegetable oils.
The group of mice consuming vegetable oils developed insulin resistance and the group consuming olive oil did not. This study is fascinating because carbohydrates played no role in the induction of insulin resistance.
Another study showed that vegetable oils damage the GLUT4 transporter, which ultimately reduces the efficacy of insulin [*], while this study showed that soybean oil was a more potent inducer of diabetes than fructose — one of the most commonly suspected causes.
It’s like ranking between the damage caused by heroin, crack, and meth. Seed oils may just be the worst offender of almost any junk you can eat.
As we discussed in a previous article, there’s no such thing as good and bad cholesterol. What’s bad is when good cholesterol gets damaged. Cholesterol is one of the most vital molecules, which is why your body produces so much every day (in fact over 70% of your cholesterol is produced endogenously).
How do you damage your cholesterol particles? Sugar and vegetable oils. Two of the first things you cut out on the carnivore diet.
How do vegetable oils damage cholesterol particles?
Lipoproteins like LDL, the floaties that carry around fats and cholesterol in your body, are more prone to oxidation when they’re carrying linoleic acid (LA) as cargo. It’s like a plane that’s more likely to crash because all the passengers are drunk (not necessarily true…).
Once LDL is oxidized, LDL receptors no longer recognize it. Instead, the immune system takes over. When LDL is oxidized, your body intentionally pulls it into your artery walls to prevent them from causing damage elsewhere [*].
These damaged lipoproteins will then cause an inflammatory response, foam cells, and plaquing. Macrophages basically ingest the modified LDL and turn into foam cells. Over time, these foam cells form fatty streaks and ultimately can turn into atherosclerotic plaque.
Yes, cholesterol is present when there is plaquing that causes heart disease. But it is generally this oxidized cholesterol.
Another recently unearthed clinical trial that tried to test the diet heart hypothesis backfired.
Data from the Minnesota Coronary Experiment conducted by Ancel Keys was unearthed in 2017 after 40 years of sitting dormant.
It was one of the most comprehensive to date: randomized and controlled with 9,400 participants.
The control group continued to eat a diet high in saturated fats and animal fats. The intervention group ate a serum cholesterol lowering diet that replaced saturated fat with vegetable oils (from corn oil and corn oil polyunsaturated margarine).
Results: the intervention group had a 14% reduction in cholesterol but a 22% increase in mortality.
This should have been the nail in the coffin for the diet-heart-hypothesis, but it was completely buried. Cholesterol went down, while deaths went up. Likely because of the increased ox LDL content.
We’ve had our eye on the wrong ball all along. Oxidized cholesterol, not healthy cholesterol, causes heart disease. This is why the level of oxidized LDL is one of the best biomarkers for heart disease. [*]
The great lengths people go to stay young. If only they would cut out vegetable oils and start fasting, they wouldn’t need to spend tens of thousands of dollars on facial rejuvenation, botox, and Beverly Hills plastic surgeries.
What is aging?
Aging is a mitochondrial disease, characterized by increased inflammation, oxidative stress and reduced autophagy (the cellular cleansing process). Over time it’s natural to age, but vegetable oils accelerate all three processes.
As discussed above, the high omega 6 content in vegetable oils disrupt our natural omega 6 : omega 3 ratio and encourage a pro inflammatory state. This chronic low grade inflammation accelerates the aging process. Whereas diets higher in omega 3 fats reduce aging and increase mitochondrial efficiency.
And this is where the vicious cycle begins…as you experience chronic low grade inflammation your mitochondria gets damaged and produces free radicals that end up accelerating damage further.
As you age, the balance between healthy and dysfunctional mitochondria is disrupted.
As discussed above, one of the most pernicious effects of vegetable oil consumption is mitochondrial mutation. Just 4 weeks of increased consumption of vegetable oils causes mitochondria in rates [*].
Lastly, most people eating vegetable oils are also eating 6+ meals a day (i.e. grazing). This shuts off autophagy, and prevents their body from cleaning out the dysfunctional mitochondria and generating new ones.
More evidence continues to emerge that the caloric theory of obesity is about as right as the earth is flat.
Food is a signaling molecule. Different fatty acids and their metabolites (byproducts) change everything from hunger to fat accumulation.
Recent studies have shown that exposing mice to a high omega 6 diet results in the accumulation of body fat across generations. This study showed that each generation that consumed omega 6s became fatter than the previous.
Why? For one, HNE triggers fat accumulation by altering fat tissues. This study in C. Elegans — a yeast — showed that HNE signaled to cells that they should be storing fat instead of burning it.
Another study in rats tested 3 diets composed of varying amounts of soybean oil. The percentages ranged from 1% to 22%, which is representative of the western diet.
Calories were identical but all three test groups gained more than twice the amount of weight. Just 1% of calories from linoleic acid can induce weight gain. There is no such thing as moderation here…
Whereas Omega 3 acids encourage beta oxidation — burning fat for fuel — omega 6 fatty acids suppress it [*].
Beware. Vegetable oils are now hiding everywhere.
Vegetable oils are now hiding absolutely everywhere. Everything from salad dressings, to pasta, to cereal and chips all are loaded with these vegetable oils. You’d be hard pressed to find anything without them in a grocery store.
If you’re unaware of this issue it’s extremely difficult to avoid them.
This has been the single biggest change to our health over the last 100 years…and there have been a lot.
You need to be on the lookout for these health nuclear bombs. Instead, eat tallow. One of the most nutritious foods there is.
There are now so many ingrained interests in ensuring this ball keeps rolling down hill. The people making millions selling these “heart healthy oils”. The doctors treating the consequences of the damage. The pharmaceutical companies making drugs to dampen the blow. There are way too many Mercedes and private school educations on the line here to turn this ship around.
But each of us has it in our own power to take back control of our health. The first step starts with removing this poison from our diet.
After removing all the junk from your diet, replace it with the most nutritious food in the world — animal products.
Next time you bite into a slice of watermelon or a cob of corn, consider this: These familiar fruits and veggies didn’t always look and taste this way.
Genetically modified foods, or GMOs, inspire strong reactions nowadays, but humans have been tweaking the genetics of our favorite produce for millennia.
While GMOs may involve splicing genes from other organisms (such as bacteria) to give plants desired traits — like resistance to pests, selective breeding is a slower process whereby farmers select and grow crops with those traits over time.
From bananas to eggplant, here are some of the foods that looked totally different before humans first started growing them for food.
This 17th-century painting by Giovanni Stanchi depicts a watermelon that looks strikingly different from modern melons, as Vox points out. A cross-section of the one in the painting, which was made between 1645 and 1672, appears to have swirly shapes embedded in six triangular pie-shaped pieces.
Over time, humans have bred watermelons to have a red, fleshy interior — which is actually the placenta — like the ones seen here. Some people think the watermelon in Stanchi’s painting may just be unripe or unwatered, but the black seeds in the painting suggest that it was, in fact, ripe.
The first bananas may have been cultivated at least 7,000 years ago — and possibly as early as 10,000 years ago — in what is now Papua New Guinea. They were also grown in Southeast Asia. Modern bananas came from two wild varieties, Musa acuminata and Musa balbisiana, which had large, hard seeds, like the ones in this photo.
The hybrid produced the delicious modern banana, with its handy, graspable shape and peelable covering. Compared to its ancestor, the fruit has much smaller seeds, tastes better, and is packed with nutrients.
Throughout their history, eggplants have come in a wide array of shapes and colors, such as white, azure, purple, and yellow — like those shown here. Some of the earliest eggplants were cultivated in China. Primitive versions used to have spines on the place where the plant’s stem connects to the flowers.
But selective breeding has gotten rid of the spines and given us the larger, familiar, oblong purple vegetable you find in most grocery stores.
The earliest known carrots were grown in the 10th century in Persia and Asia Minor. These were thought to originally be purple or white with a thin, forked root — like those shown here — but they lost their purple pigment and became a yellow color.
Farmers domesticated these thin, white roots, which had a strong flavor and biennial flower, into these large, tasty orange roots that are an annual winter crop.
Perhaps the most iconic example of selective breeding is North American sweetcorn, which was bred from the barely edible teosinte plant. Natural corn, shown here, was first domesticated in 7,000 BC and was dry like a raw potato, according to this infographic by chemistry teacher James Kennedy.
Today, corn is 1,000 times larger than it was 9,000 years ago and much easier to peel and grow. Also, 6.6% of it is made up of sugar, compared with just 1.9% in natural corn, according to Kennedy. About half of these changes occurred since the 15th century, when European settlers started cultivating the crop.
Peaches used to be small, cherry-like fruits with little flesh. They were first domesticated around 4,000 B.C. by the ancient Chinese and tasted earthy and slightly salty, “like a lentil,” according to Kennedy.
But after thousands of years of farmers selectively breeding them, peaches are now 64 times larger, 27% juicier, and 4% sweeter.
So next time someone tells you we shouldn’t be eating food that’s been genetically modified, you can tell them we already are.
Source: Article by Tanya Lewis (https://www.businessinsider.com/what-foods-looked-like-before-genetic-modification-2016-1)
3) A study in Framingham, MA 60 years ago claimed cholesterol led to heart disease [*].
All three ultimately led to the diet-heart hypothesis and Food Pyramid.
Cholesterol was the critical second link of the diet-heart hypothesis. The hypothesis was that saturated fat increased cholesterol. And based on the studies above, that cholesterol then caused heart disease.
After cholesterol was found to be present in artery walls in patients with heart disease, cholesterol was blamed as the cause of the disease.
But we convicted the wrong enemy.
The Truth About Cholesterol
All three studies used to convict cholesterol would turn out to be flawed and corrupt.
The 1913 study on cholesterol by the russian scientist was on rabbits. Rabbits are herbivores. Of course they react negatively to cholesterol.
Ancel Keys cherry picked seven countries out of 22. After including all the countries there was no correlation.
There was not a shred of truth in any of the three studies.
A 30 year follow up to framingham actually showed a negative correlation between cholesterol and disease.
“There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels).” [*]
So of course the USDA and health authorities backtracked on their cholesterol recommendations and saturated fat vilification right…? Of course not. They doubled down and still recommend people limit saturated fat.
Studies Confirm LDL and Total Cholesterol Are Not Risk Factors
Now that cholesterol has been rigorously tested, more studies continue to emerge that cholesterol is not predictive of heart disease.
In 1987, a thirty year follow up to the Framingham study was conducted — the study that crucified total cholesterol in the first place.
Those aged between 48 and 57 with cholesterol in the mid range (183-222 mg/dL) had a greater risk of heart attack than those with higher cholesterol.
They also found that “for each 1 mg/dL per year drop in serum cholesterol values, there is an 11% increase in both the overall death rate and the CVD death rate.” [*]
In fact, there are zero studies that show that high LDL is a risk factor, independent of triglyceride levels and HDL levels. [*]
What matters is the functioning of your lipid and energy transport system.
And a big reason why there is often a correlation between LDL, HDL and heart disease is because they are potentially indicative of a broken system.
And you know what? New scientific research confirms this.
There’s not a single randomized control trial that shows people with high LDL die younger. David Diamond has done some great work here.
In fact, some studies show that higher LDL-C is associated with equal or greater lifespan [*].
When it comes to total cholesterol, a study in Hawaii found the same. Having low cholesterol for a long time actually increases risk of death:
Instead of continuing to dig their heels in, I do appreciate the honesty of the study above: “we have been unable to explain our results”.
This study from UCLA showed that 75% heart disease patients had LDL below 130 mg/dl — the level at which doctors prescribe statins.
The above data shows that saturated fat can raise cholesterol. But no evidence has shown that, independent of other factors, high cholesterol is a cause for concern.
New evidence continues to pile up that cholesterol alone is not the culprit when it comes to heart disease. And that lowering it is not necessarily beneficial (in fact in some cases it can cause more damage).
In 2019, the BMJ reviewed 22 interventional trials and found that “‘The preponderance of evidence indicates that low-fat diets that reduce serum cholesterol do not reduce cardiovascular events or mortality” [*]
In the recently unearthed Minnesota Coronary experiment researchers lowered cholesterol like they intended by 14%.
But this led to a “22% higher risk of death for each 30 mg/dL reduction in serum cholesterol”
This study was BURIED for 40 years.
Lastly, remember the seven countries study that blamed saturated fat and cholesterol for heart disease? Well Zoe Harcombe added in 290 more countries and the correlation flipped. Cholesterol actually becomes negatively correlated with heart disease.
What BioMarkers Are Predictive of Heart Disease?
Yes, cholesterol is present in the artery walls of heart disease patients.
But it’s because it was there to rescue their artery walls.
It’s like condemning firefighters for starting fires just because they’re present at all fires. The logic is completely backwards.
What matters is how the fire started in the first place.
LDL, the “bad cholesterol”, is not predictive alone. Of course not. Because it is not inherently harmful. It’s only indicative of an atherogenic environment when it’s coupled with inflammation and oxidation.
What is the signature of inflammation and oxidation?
It usually rears its head as high TG / HDL ratios and high fasting insulin.
In a recent study of 103,446 men and women, LDL levels showed very minimal effect on heart disease.
But an increase in triglycerides/HDL ratio doubled the risk of heart disease. [*]
High triglyceride/HDL ratios are indicative of high remnant cholesterol, which is a better indicator for heart disease than LDL alone [*].
Dave Feldman showed below that remnant cholesterol correlated highly with all cause mortality.
And guess what is significantly associated with remnant cholesterol? Insulin resistance [*].
When it comes to biomarkers, I like to see:
– Total / HDL < 4
– TG / HDL < 1
– HDL > 40
– TG < 100
– Fasting insulin < 10
– Fasting glucose < 5 mmol/L
LDL, the “bad cholesterol”, is nowhere to be found…Why?
Big pharma can’t make money off the REAL predictive biomarkers
Make sure to also keep an eye on fasting insulin levels.
From the great Ivor Cummins: When insulin is low, high LDL particle count and high triglycerides don’t indicate that you’re at higher risk. [*]
But when insulin is high, the risk of high triglycerides and high LDL is magnified.
When fasting insulin is >15 uU/mL, your risk of heart disease with the same triglyceride levels go up 6.7x. And with the same LDL-P levels, it increases 11x.
High LDL with high insulin is much more concerning than high LDL with low insulin.
Too Little Cholesterol is Worse Than Too Much
Cholesterol is an organic molecule found in cell membranes and most tissues. It’s in the food we eat and is naturally occurring within our bodies.
Of the cholesterol present, around 75% is created in our bodies, and 25% is ingested.
Cholesterol is one of the most vital compounds in our bodies. So vital that our bodies make around 3000 mg of it every single day. [*] We can’t leave it to chance to get it externally – it’s that important.
Without cholesterol, we would literally be dead.
Cells would disintegrate. We’d have no hormones, no brain function, and no muscles. Every cell membrane is constructed out of cholesterol.
All of the following critical body components are made from cholesterol: [*][*]
Cortisol (anti-inflammatory stress hormone)
Aldosterone (regulates salt balance)
Bile (required for fat and vitamin absorption)
Brain synapses (neurotransmitter exchange)
Myelin sheath (insulates nerve cells)
Not having any cholesterol is MUCH worse than having too much of it.
Cholesterol is one of the most important molecules in your body. It is not a direct etiological agent in heart disease — it is merely correlative because it can indicate fundamental damage.