Ad Libitum: Was Atkins right?

Ad Libitum: Was Atkins right?

Wednesday, 23 May 2012

Was Atkins right?

About the need to go below 20 carbs for optimal results, I mean?

I've been doing my little hardcore ketogenic experiment for the last 5 days. 4 lbs gone. What shocks me about this is that normally I eat 50-60 carbs anyway and yet weight loss is so extreme and effortless on <20, as if I'm starting LC for the first time. I really need to emphasise that I'm not someone coming off of the SAD; I've been lowcarbing for over a year and I'm coming to this experiment in a severely weight-reduced state having already lost 60 lbs. It's incredible. What also shocks me is that I have a terrible case of the Atkins flu even though I have been eating at mildly or borderline ketogenic levels for at least half a year. I feel as if I'm ketoadapting for the first time. Is it possible that ZC is qualitatively different from even VLC, let alone bog-standard LC?

I should also mention I'm eating up to 1,700 calories a day on this regime and losing weight. I wonder if that will still be the case once the diuretic effect has worn off. I find that induction works in two ways: first, it kills your appetite dead after about 36 hours. After two days, I felt as if I never needed to eat again and the only reason I eat now is to prevent cardiac complications from electrolyte loss which can happen in total starvation. The second mechanism of action allows you to consume a lot more calories than you could on a balanced (carbohydrate-containing) diet and still lose weight. I seem to be wasting a lot of calories through heat. On the other hand, try eating 1,700 calories of carb a day as a female while sitting around the house all day not lifting your bum off the chair and see how you get on.

Another thing of huge importance (well, to me anyway :p) I have noticed is that it matters HUGELY where the calories come from. It's not just about eating high fat moderate protein low carb. You have to eat virtually all your calories from animals, unfortunately. Now, I just wanna preface this by saying I'm no fan of killing animals and I am not a huge meat lover at all (I used to live on pasta, rice, potato, bread, pastry and could happily eat no meat ever until my untimely demise). I hate paleo caveman carnivore bullshit BUT I must say that satiety is best when virtually no plant food is consumed. Fact. I don't know if this is a carb/insulin issue or is it the fact that things like egg yolk, beef fat, meat and liver are super nutritious and very satiating because the body gets all the essential nutrients and goes "you don't need to eat anything else today", whereas eating nutritionally empty bulk like wheat, well, you can go face down in it and eat for hours while still being hungry because you haven't actually consumed anything of value. I have been eating only two meals a day, spaced by about 5-6 hours, with absolutely zero snacking in between, of nothing but meat, butter, eggs, cheese and lettuce. I am experiencing zero hunger. Zero. It can't be boredom; it appears to be physiological. I crave sugar and crap I love, but I am not hungry. I do not need FOOD.

Now, compare and contrast this with when I used to delude myself into thinking plants were ok and that I could get away with a more varied diet of nuts, berries, yoghurt etc. on top of some meat and animal fat. Looking back on my first stall, I was still eating 65-70% fat. Yet, the hunger was there, the urge to snack on shit was there, and weight loss stalled. A bit of extra cheese here, a handful of nuts there and you're back to 2,000 calories and maintaining instead of losing.

I no longer believe I can get away with a more vegeterian version of the HFLC diet. In fact, I'm more and more evolving toward the Hyperlipid school of thought in thinking that a healthy diet can contain virtually no plant matter. I don't actually think anything except meat, eggs, fat and broth is necessary for life. There's a reason why all these LC doctors - CLINICIANS with first-hand experience of obesity treatment - always recommended basing your diet on meat. Not nuts or dairy. Meat. I would love to be able to eat a bowl of mixed nuts, berries and flax in full-fat Greek yoghurt for breakfast like I used to but it seems that I can't, for reasons that do not appear to be explained by simple macronutrient ratios. 
This is very difficult for me to accept emotionally. I mean, who wants to eat nothing but meat forever? 


Human microbiota and atherosclerosis - Lucas Tafur

Lucas Tafur: Human microbiota and atherosclerosis

We are 90% microbes and 10% human.

Monday, March 12, 2012

Human microbiota and atherosclerosis

I've been wanting to post about this study for a while now. I think its a good update while I finish my first post on my nutritional immunotherapy protocol. This study was performed given the preliminary evidence linking infections and atherosclerosis, and the association of the human microbiota with the atherosclerotic plaque. For example, bacterial DNA has been observed in atherosclerotic plaques from young and old subjects (1, 2). This relationship has been investigated with more focus on oral bacteria, due to the association of periodontal disease and cardiovascular disease (CVD) (3, 4) and the presence of periodontal pathogens in  atherosclerotic plaques (5). 

The authors tried to answer the following questions:

Is there a core atherosclerotic plaque microbiota? 
Are bacteria present in the plaque also detectable in the oral cavities or guts of the same individuals?
Do the microbiotas of the oral cavity, gut, and atherosclerotic plaque relate to disease markers such as plasma levels of apolipoproteins and cholesterol? 
Is an altered oral or fecal microbiota associated with atherosclerosis?

Using 16S rRNA sequences (from patients with clinical atherosclerosis and controls) and the unweighted UniFrac distance metric (qualitative instead of quantitative), they found strong clustering of samples according to body site, suggesting that the oral, gut and atherosclerotic plaque (AP) sites have different microbial communities:

PC1 and PC2 refer to the first two principal coordinates from the principal coordinate analysis of unweighted UniFrac, plotted for each sample (See also Fig S1). Of these sites, bacterial diversity was higher for the gut microbiota. 

The analysis of the atherosclerotic plaque microbiota revealed that there was a positive correlation between the amount of bacterial 16S rRNA and the number of leukocytes present in the AP, and there was significantly higher levels of Proteobacteria and fewer Firmicutes compared with the oral and gut samples. Supporting the role for a "core" AP microbiota, several OTUs were present in all AP samples, which differentiated these samples from oral or fecal samples: Chryseomonas was detected at high levels in the AP samples, but not in gut or oral samples, being the most discriminative genus between sites and driving the differences between body sites. Other OTUs, three for the genus Staphylococcus, three classified as Propionibacterineae and one belonging to the genus Burkholderia, were specific for AP samples and were present in all AP samples analyzed.

There were no OTUs differentiating oral samples from healthy subjects and patients, but there were correlations between the abundances of OTUs in the oral cavity and CVD markers: the abundance of Fusobacterium was positively correlated with levels of cholesterol (P = 0.028) and LDL (P = 0.005), the abundance of Streptococcus was positively  correlated to HDL (P = 0.0001) and ApoAI (P = 0.01) levels and the abundance of Neisseria was negatively correlated to levels of these last two markers (P = 0.02 and 0.005, respectively). This is interesting, given that Fusobacterium has been associated with periodontal disease (6). As with oral samples, there were no differentiating OTUs between gut samples from controls and patients (in terms of OTU abundances). In gut samples, the abundance of two OTUs classified as uncharacterized members of Erysipelotrichaceae and Lachnospiraceae families were positively correlated with cholesterol (P = 0.009 and 0.001, respectively) and LDL (P = 0.012 and 0.007, respectively). 

Finally, inter-individual comparisons between sites showed that some OTUs were shared among sites. These included OTUs for Veillonella (in AP and oral samples in 11 of 13 patients, detected also in the gut sample of two patients) and Streptococcus (in AP and oral samples in 6 of 10 patients, detected also in the gut of four patients). Within patients, the AP samples contained OTUs shared with oral (Propionibacterium, Rothia, Burkholderia, CorynebacteriumGranulicatella, Staphylococcus) and gut (BacteroidesBryantella, EnterobacterRuminococcus) samples. 

  • The study identified a "core" atherosclerotic plaque microbiota, comprising higher levels of Proteobacteria and fewer Firmicutes, compared with the gut and oral samples. 
  • The AP microbiota contained specific OTUs not shared with the analyzed body sites.
  • The abundance of some OTUs in the gut and oral cavity was correlated with CVD markers. 
  • Shared OTUs among sites included Streptococcus and Veillonella, the correlation being stronger among the oral cavity and the AP, and these OTUs were also found in the gut samples from some patients. Across patients, the abundance of both were correlated in the oral cavity and the AP.

I find this study very interesting because it supports the role of infection on the pathogenesis of atherosclerosis and CVD. The "infection hypothesis" of atherosclerosis has been proposed before (7). The fact that specific bacteria is present in AP and not in other body sites analyzed and that the amount of bacterial 16S rRNA was positively correlated with leukocyte counts, support the notion that these pathogens support directly atherosclerosis progression. However, the study only analyzed the oral cavity and the gut, so it is impossible to conclude that these pathogens couldnt have been derived from other body sites (for example, the skin). Moreover, primers commonly utilized to amplify 16S rRNA sequences are limited to some species, an inherent property of the method (8). Nevertheless, it seems more feasible to suppose that the origin of AP bacteria is the oral cavity because of the close proximity of the bacterial communities in the mouth to the highly vascularized gingival lining and because of the thickness of the subgingival epithelium, which differs from other protective layers such as the skin or the gut mucosa (9). Accordingly, any mechanical disruption of oral bacterial biofilms can trigger bacteremia, and these include oral procedures (periodontal probing, tooth extractions, etc), oral hygiene activities (such as brushing) and physiological phenomena (like chewing) (9). This, coupled with the findings that the abundance of OTUs in the AP were correlated with that of the oral cavity support this hypothesis. Gut bacterial origin is more complicated but feasible (as shown by the presence of gut bacteria in AP samples). The authors suggest that one possible way of this transfer is by phagocytosis of macrophages at epithelial linings. 

If indeed bacteria play a role in the formation and/or progression of atherosclerosis, the million dollar question is why do these specific pathogens adhere to the vascular endothelium? Moreover, is this colonization the initial trigger for the localized inflammatory response or just aggravates the condition? With the available evidence it is hard to answer these questions. It has been proposed that atheromas might act as mechanical sieves, collecting bacteria from the cirulation (10). This would have deleterious consequences, as bacterial accumulation in the AP would lead to an increased inflammatory response. It could also link the fact that endotoxemia increases the risk of CVD (11), for which periodontal pathogens seem to play an important role (12). Supporting the role of infection as secondary to atherosclerotic inflammation, fungal DNA has been observed in AP (13), with some species correlated with that found on human microbial communities. It is of worth noting that in this study, fungal richness was not associated with classical CVD risk factors. Because not all normal residing oral bacteria are found in AP samples, AP invasion might be related to the virulence properties of some species (9). This seems to be the case, as in the study reviewed here, there was a common abundance of Streptococcus and Veillonella in AP samples. Streptococcus is able to adhere to the endothelium, while Veillonella is able to change its adherence capacity in the presence of some factors from Streptococcus (14). In fact, there is a tight relationship between Streptococcus and Veillonella in the oral cavity as some strains co-aggregate, partially because Veillonella seems to be metabolically dependent on Streptococcus (15). This relationship is so important that Veillonella is unable to establish an infection without Streptococcus.

In conclusion, microbial accumulation in AP might contribute to the progression of atherosclerosis. Although the mechanism by which these microorganisms colonize this site is not defined, it is clear that several microbes found in other body sites are also found in AP, which suggests that the normal human microbial communities are an important source of pathogens contributing to atherosclerosis progression. Translocation from these sites, in turn, is controlled by the host inflammatory status. This seems to be relevant to translocation from the oral cavity: transient bacteremia is experienced by everyone because of mechanical disruption of microbial biofilms (for instance, when eating), but it is controlled quickly. However, there are always some persisters which resist by-standing immune mechanisms. Obviously, a higher microbial load facilitates dissemination into the bloodstream and could possible influence the degree of transient bacteremia. A higher bacterial load coupled with a compromised subgingival epithelium barrier increases the risk of bacteremia and secondary colonization. So, in order to reduce the risk of AP colonization by oral pathogens, it is wise to target these two factors. For reducing oral bacterial load (overgrowth), reducing sucrose intake might be of benefit, as bacterial glucosyltransferase (GTF) plays a crucial role in plaque formation (16) and S.mutans is only pathogenic in the presence of sucrose (17). Dietary sucrose has been shown to increase total viable microbial density and S.mutans population in human dental plaque (18). Sucrose alone seem to be more cariogenic than sucrose plus fructose (19, 20). Additionally, sucrose alters the ionic concentration in the biofilms' matrix, altering the normal de- and re-mineralization process of enamel and dentin  (21). The role of starches in dental plaque formation is controversial (22), although some authors are in agreement with the Cleave & Yudkin hypothesis, which states that an excess of fermentable carbohydrate intake (in the absence of dental interventions) promotes dental diseases and then systemic diseases (23). Nevertheless, starchy foods commonly ate might promote dental plaque formation and disease. Pollard (24) showed that cornflakes, branflakes and wholemeal bread produced the minimum dental plaque pH peak, while all foods tested promoted enamel demineralization*. This might be related to the fact that, although starches can reduce plaque pH and induce demineralization, sucrose accelerates this effects (25). This is probably mediated by the interaction between bacterial GTF and salivary amylase (26). In contrast to what some might expect, whole fruit and fruit juices induce enamel demineralization by the same magnitude (27). This has been also found in some observational studies, where high fruit consumption is associated with increased caries risk (28). On the contrary, cheese and nuts have shown a negative association (29). Finally, inflammation increases the risk of oral bacterial growth and translocation, which might induce and/or aggravate systemic diseases (30). Periodontal disease has been positively associated with obesity (31), metabolic syndrome (32), type 2 diabetes (33), Alzheimer's disease (34), among other. Thus, controlling inflammation is key to avoid secondary diseases caused by pathogenic oral bacteria. 

* "Test foods were oranges, apples, bananas, Cornflakes, Branflakes, Weetabix, Alpen (no added sugar), white bread, wholemeal bread, rice, and spaghetti, with positive and negative controls of sucrose and sorbitol."

ResearchBlogging.orgKoren O, Spor A, Felin J, Fåk F, Stombaugh J, Tremaroli V, Behre CJ, Knight R, Fagerberg B, Ley RE, & Bäckhed F (2011). Human oral, gut, and plaque microbiota in patients with atherosclerosis. Proceedings of the National Academy of Sciences of the United States of America, 108 Suppl 1, 4592-8 PMID: 20937873


Health Correlator: Rice consumption and health

Health Correlator: Rice consumption and health

Monday, May 21, 2012

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Carbohydrate-rich foods lead to the formation of blood sugars after digestion (e.g., glucose, fructose), which are then used by the liver to synthesize liver glycogen. Liver glycogen is essentially liver-stored sugar, which is in turn used to meet the glucose needs of the human brain – about 5 g/h for the average person.

(Source: Wikipedia)

When one thinks of the carbohydrate content of foods, there are two measures that often come to mind: the glycemic index and the glycemic load. Of these two, the first, the glycemic index, tends to get a lot more attention. Some would argue that the glycemic load is a lot more important, and that rice, as consumed in Asia, may provide a good illustration of that importance.

A 100-g portion of cooked rice will typically deliver 28 g of carbohydrates, with zero fiber, and 3 g of protein. By comparison, a 100-g portion of white Italian bread will contain 54 g of carbohydrates, with 4 g of fiber, and 10 g of protein – the latter in the form of gluten. A 100-g portion of baked white potato will have 21 g of carbohydrates, with 2 g of fiber, and 2 g of protein.

As you can see above, the amount of carbohydrate per gram in white rice is about half that of white bread. One of the reasons is that the water content in rice, as usually consumed, is comparable to that in fruits. Not surprisingly, rice’s glycemic load is 15 (medium), which is half the glycemic load of 30 (high) of white Italian bread. The glycemic load of 100 g of baked white potato is 10 (low).

The glycemic load of a portion of food allows for the estimation of how much that portion of food raises a person's blood glucose level; with one unit of glycemic load being equivalent to the blood glucose effect of consumption of one gram of glucose.

Two common denominators between hunter-gatherer groups that consume a lot of carbohydrates and Asian populations that also consume a lot of carbohydrates are that: (a) their carbohydrate consumption apparently has no negative health effects; and (b) they consume carbohydrates from relatively low glycemic load sources.

The carbohydrate-rich foods consumed by hunter-gatherers are predominantly fruits and starchy tubers. For various Asian populations, it is predominantly white rice. As noted above, the water content of white rice, as usually consumed by Asian populations, is comparable to that of fruits. It also happens to be similar to that of cooked starchy tubers.

An analysis of the China Study II dataset, previously discussed here, suggests that widespread replacement of rice with wheat flour may have been a major source of problems in China during the 1980s and beyond (1).

Even though rice is an industrialized seed-based food, the difference between its glycemic load and those of most industrialized carbohydrate-rich foods is large (2). This applies to rice as usually consumed – as a vehicle for moisture or sauces that would otherwise remain on the plate. White rice combines this utilitarian purpose with a very low anti-nutrient content.

It is often said that white rice’s nutrient content is very low, but this problem can be easily overcome – a topic for the next post.


Tuck said...
"Two common denominators between hunter-gatherer groups that consume a lot of carbohydrates and Asian populations that also consume a lot of carbohydrates are that: (a) their carbohydrate consumption apparently has no negative health effects; and (b) they consume carbohydrates from relatively low glycemic load sources." I think that (a) is a pretty big assumption. The Chinese seem to be having all the same health issues that we do, now that they're regularly getting enough to eat: "China diabetics raise stakes for healthcare reform" I'm inclined to agree with you, since I suspect that the real issue is what and/or linoleic-acid-rich seed oils, but I don't feel comfortable yet exonerating carbs.
Ned Kock said...
Hi Tuck. In the China Study post that I linked (link below as well), the effect may indeed be due to other factors (e.g., rice consumption being correlated with wealth). http://bit.ly/aW4XNa But the fact that the health effect of rice consumption is there even when we control for total calorie intake goes against the main premise of that Reuters article you provided (thanks!) on diabetes in China. Omega 6 fats overload cannot be excluded as a possible major confounder, but I’d be tempted to exclude calorie intake per se as a factor based on the China Study analysis.


AJCN Publishes New PUFA Study That Should Make Us Long For the Old Days - The Daily Lipid:

The Daily Lipid: AJCN Publishes New PUFA Study That Should Make Us Long For the Old Days

Thursday, May 17, 2012

I have a new post over at Mother Nature Obeyed:
This is my response to the new study published in AJCN showing that replacing butter with sunflower oil decreases liver fat, PCSK9, and improves a handful of metabolic markers.  I begin with a critical review of the 2010 meta-analysis by Mozaffarian and colleagues claiming that the randomized, controlled trials substituting vegetable oils for saturated fats show that this swap reduces heart disease risk, which was cited by the AJCN authors in justification of their research approach.  I then move on to reviewing the animal evidence suggesting that saturated fats increase fatty liver in certain contexts while polyunsaturated fats do so in others.  I conclude by reviewing the AJCN study and lamenting its irrelevance.  I suppose this is quite long for an analysis of a study I finally conclude is irrelevant, but I hoped we might all learn a few things (especially including myself!) and perhaps score a chuckle or two in the process. 


China diabetics raise stakes for healthcare reform | Reuters

China diabetics raise stakes for healthcare reform | Reuters

A young boy suffering from diabetes is held by his mother as he has his tongue checked by diabetes specialist Doctor Tong Xiao Lins at the Guanganmen Chinese medicine Hospital in Beijing March 19, 2012. In 30 years, the Chinese people have gone from having barely enough to eat to worrying about chronic diseases like diabetes, leaving the healthcare system struggling with a condition that is rapidly outpacing its ability to keep up. Spending on diabetes reached $25 billion in China in 2010, only 6 percent of the $390 billion spent worldwide. But the rate of diabetes in China is already at the same levels as in the West, leaving doctors, drug companies and policymakers to hunt for low-cost alternatives before the disease swamps the rudimentary healthcare system. Picture taken March 19, 2012. REUTERS-David Gray

BEIJING | Sun Mar 25, 2012 3:29am EDT
(Reuters) - In 30 years, the Chinese people have gone from having barely enough to eat to worrying about spreading waistlines, leaving the healthcare system struggling to keep up with an exponential rise in "nobleman diseases" like diabetes.

The soaring cost of chronic disease could tax China's effort to offer basic healthcare to 1.4 billion people. Almost one out of every eight Chinese households was racked by catastrophic health expenses in 2011, according to a paper published in medical journal The Lancet.
Healthcare reform is needed to rebalance the economy, since Chinese salt away their savings in part because of fear of being wiped out by devastating illness.

But the burden of chronic illnesses could worsen as Chinese eat more and live longer. Diabetes, for instance, now afflicts nearly 10 percent of Chinese adults - roughly the same proportion as in the United States - up from 1 percent in 1980.

"In the last 20 years, diabetes has developed a lot, but it's only now showing up in the medical system," said Dr Tong Xiaolin, vice director of the Guanganmen Hospital in Beijing, who sees dozens of patients during Monday office hours.

"People are now just flooding into the system in real numbers. The next 10 years will be a real drain on the system."

Spending on diabetes reached $17 billion in China in 2011, a tiny amount compared with the $465 billion spent worldwide, according to a white paper from Singapore's Saw Swee Hock School of Public Health and the Harvard School of Public Health.

That represents about 5 percent of total healthcare spending in China, with some estimates rising to 13 percent.

In the United States, where costs have ballooned, diabetes accounts for about $1 in every $10 spent on healthcare, according to the American Diabetes Association. Spending on diabetes at U.S. levels of $201 billion a year would swamp China's system, leaving it unable to tackle other priorities.

There are now about 92 million diabetics in China but that is expected to rise to 130 million by 2030.

"We were very surprised and couldn't believe how fast it grew," said Peking Union Medical College Hospital specialist Xiang Hongding, as he sipped coffee after a typical morning spent seeing 22 patients in four hours.

The rapid growth means diabetes often goes unrecognised until secondary symptoms appear, making treatment much harder.

Liu Yuxiang travels five hours to Beijing every month to see Dr Tong, and reckons she has spent 30,000 yuan ($4,700) on Chinese medicines to treat painful and swollen legs. Western drugs to control blood sugar cost her another 12,000 yuan a year, 80 percent of which is covered by insurance.

"If we didn't have a doctor in the family I would never have known. No one around us had any knowledge of it," said the cheerful 64-year-old, who suffered from years of thirst, fainting fits and hospitalization before her daughter-in-law suggested she might have diabetes.
Many doctors, especially in the countryside, have no inkling that diabetes could be the underlying cause for a number of symptoms -- including blindness, numb or tingling legs, digestive disorders and circulatory problems.

"Diabetes is very easy to diagnose, but even so, most doctors don't know how to do that," said Xiang, 68, who got his early medical training during China's tumultuous Cultural Revolution and now teaches rural doctors in diabetes diagnosis.
"The patients don't know, and when they get to us they say the doctors didn't know."


A nationwide insurance roll-out, begun three years ago, makes people more likely to see doctors and makes treatment much more affordable. Almost nine percent of people stayed in a hospital in 2011, from less than four percent in 2003, the study published in The Lancet showed.

Basic medicine to keep diabetes under control is relatively cheap in China, at about 2,000 yuan ($320) a year.

A diabetes patient rests his arm on a table for diabetes specialist Doctor Tong Xiao Lin (C) during a medical check-up at the Guanganmen Chinese medicine Hospital in Beijing March 19, 2012. In 30 years, the Chinese people have gone from having barely enough to eat to worrying about chronic diseases like diabetes, leaving the healthcare system struggling with a condition that is rapidly outpacing its ability to keep up. Spending on diabetes reached $25 billion in China in 2010, only 6 percent of the $390 billion spent worldwide. But the rate of diabetes in China is already at the same levels as in the West, leaving doctors, drug companies and policymakers to hunt for low-cost alternatives before the disease swamps the rudimentary healthcare system. Picture taken March 19, 2012. REUTERS-David Gray
But treatment for a patient who has developed advanced symptoms could easily reach 18,000 yuan a year, roughly equal to the average yearly income of urban Chinese.
Common drugs for diabetes are covered by insurance, but equipment for at-home testing and monitoring of blood sugar levels - which can reach 400 yuan a month - is not.

Adding to the burden, Asians in their prime earning years of 30-50 are more likely to develop diabetes than Caucasians, according to the Saw Swee Hock white paper on diabetes.
"When I found out, my heart was very heavy. I worried I wouldn't be able to support my family. I was afraid I couldn't function in this economy," said patient Wang Yuanqing, father of an 8-year-old, whose diabetes weighs heavily on him even though he has kept it under control since his diagnosis a year ago.

Catching diabetes early could help drug makers like Novo Nordisk, the top seller of insulin in China, or Bayer, which markets a drug that helps reduce glucose absorption after meals. Both help educate on diabetes in China.

(Additional reporting by Tan Ee Lyn in HONG KONG; Editing by Paul Tait)

Why I Recently Gave Up Eating Bacon on the Paleo Diet » Your source for Paleo Diet information

Why I Recently Gave Up Eating Bacon on the Paleo Diet » Your source for Paleo Diet information

I know what you’re thinking, and yes I really did it. Those of you that know me know that I was one of the biggest proponents for the tasty, salty treat. For a long time, bacon was basically a staple for me. Most days I ate bacon several different times throughout the day. I read articles that espoused the reasons why bacon is far from an optimal food, and articles that told of the virtues of bacon. I even posted an article or two about the safety of the nitrates in our store bought bacon supply. Little did I know that one day, I would turn against the very thing I held dear for so long.

But….that day has come.

The simple truth is that pork, generally as a meat, is not a very healthy choice. On one side of the scale, it’s all relative, and choosing pork over something like bread or pasta is of course a very good idea. If someone were switching from the S.A.D (Standard American Diet), to a low-carb type of deal, they would do well to eat all of the bacon their heart desires. They will almost certainly lose weight, and their lipid numbers will improve. But, for someone who is really dialing in his or her diet to a Primal or Paleo approach, pork falls pretty far down the list as far as nutrition and overall quality goes.

It seems I’ve been pulling references from the Perfect Health Diet site a lot recently, but Paul seems to be good about publishing articles with reasonable frequency, and he just honestly makes a whole ton of sense. On February the 8th 2012, Paul published an article about pork, called “Pork: Did Leviticus 11:7 Have it Right?”. I think this fits right in with the reasons why I recently gave up eating bacon on the Paleo diet.
“If we were to rank popular meats by their healthfulness, the order would be (1) fish and shellfish, (2) ruminants (beef, lamb, goat), and (3) birds (duck, chicken, turkey). In last place would be pork.

Given the iconic place of bacon in the Paleo movement, it’s worth exploring the evidence against pork.  George Henderson has given us a great place to start:  “Nanji and Bridges identified possible problems with pork plus moderate alcohol in 1985 and other researchers have confirmed the pattern since.”
I think that any knowledgeable Paleo diet practitioner would argue Paul’s point that bacon is iconic within the Paleo movement. I don’t believe that anyone actually thinks that bacon is an optimal food…..but it is yummy!

“Pork Consumption and Liver Cirrhosis

Pork consumption has a strong epidemiological association with cirrhosis of the liver. Startlingly, pork may be even more strongly associated with alcoholic cirrhosis than alcohol itself!

The evidence was summarized by Francis Bridges in a recent (2009) paper [1], building on earlier work by Nanji and French [2]. A relation between pork consumption and cirrhosis of the liver is apparent across countries and has been consistently maintained for at least 40 years.”

“In epidemiological studies, beef, lamb, and pork are often grouped together as “red meat.” However, this may conceal differences between pork and the ruminant meats. Bridges found that beef actually appeared protective against cirrhosis”

“This would be consistent with considerable evidence, discussed in our book (pp 57-58), showing that saturated fat is protective against liver disease, while polyunsaturated fat causes it. Epidemiological data confirms that saturated fat is protective”

“Beef is high in saturated fat, low in polyunsaturated fat. Pork is relatively high in polyunsaturated fat.

If the fat composition is playing a role, perhaps it is not that surprising that pork is more strongly related to cirrhosis than alcohol.

Either fructose or alcohol can react with polyunsaturated fat to produce liver disease. Sugar consumption, for example in soft drinks, may be just as likely to combine with pork to cause a cirrhotic liver as alcohol. But no other common dietary component can substitute for the role of polyunsaturated fat in causing liver disease.”
This makes a lot of sense, and fits right in with what Ray Peat says about the negative interaction between Polyunsaturated fat and Fructose in the diet. Peat says that Fructose by itself is actually beneficial, but when intake of PUFA is also significant, people can quickly develop fatty liver disease.

“Pork and Liver Cancer

We would expect that if pork can cause liver cirrhosis it will also promote liver cancer, since injured and inflamed tissues are more likely to become cancerous.
Indeed, there is an association between pork consumption and the primary liver cancer, hepatocellular carcinoma.”

“Pork and Multiple Sclerosis

Nanji and Norad [4] looked for other diseases that correlate with pork consumption, and hit upon multiple sclerosis. The connection is remarkable:
A significant correlation was obtained between prevalence of multiple sclerosis and … pork consumption (r = 0.87, p less than 0.001). There was no significant correlation with beef consumption. [4]

As noted earlier, a correlation coefficient of 0.87 is extremely high, and a p-value below 0.001 also shows a very strong relationship. MS is much more likely to befall pork eaters. Such a strong correlation makes it look like pork, or something found in pork, is the cause of MS.

Nanji and Norad further note that beef, the “other red meat,” is not associated with MS”


There are remarkably strong correlations between pork consumption and liver disease, liver cancer, and multiple sclerosis.

What can be behind those relationships? The relatively high omega-6 fat content of pork may be a contributing factor, but it can’t be the whole story. It seems there is something else in pork that makes pork consumption risky.

What is it about pork that is so dangerous, and what does it mean for our dietary advice? That will be the topic of my next post.”

Hopefully, you now know why I recently gave up eating bacon on the Paleo diet. Already knowing that pork is very high in Omega-6 Polyunsaturated Fatty Acids was enough to convince me to give up the “hog”, but reading information like this really seals the deal for me. Again, it all makes a lot of sense, and I don’t know about you, but I can’t wait to read about what it is in pork, that Paul believes sets it apart from other meats in it’s potentially unhealthy nature.
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What If Sugar Doesn’t Cause Diabetes? » Your source for Paleo Diet information

Paleo Diet: What If Sugar Doesn’t Cause Diabetes? » Your source for Paleo Diet information

Diabetes Symbol
The Universal Symbol of Diabetes

It’s a serious question. What IF sugar doesn’t cause diabetes? I know, everyone in the world “knows” that diabetes is a functional breakdown of the body’s ability to effectively utilize and remove excess sugar (Glucose) from the blood stream, but does that mean that sugar is at the very root cause of the disease?

Isn’t that basically like saying, “The house obviously burned down, but what caused it? Well, it was simply a case of too much fire”. Is that logical? We know that the fire burned the house down, but who or what started the fire? Isn’t that the more important question?

The modern view of diabetes has been that the body loses it’s ability to clean an ever increasing amount of glucose from the blood, because cells throughout the body become resistant to an ever increasing amount of insulin in the blood. The glucose has nowhere to do, and therefore builds to toxic levels in the blood. The cycle continues, until the person becomes a full-on Diabetic and loses the ability to consume carbohydrates without the aid of medication.

Too many carbohydrates, especially of the refined variety, over a long period of time, leads to insulin resistance, which leads to obesity (usually, but not always), and then to diabetes. It all sounds logical, neat and plausible, but it may well not be correct at all.

Have you ever heard of the Randle Cycle?
“The Randle cycle is a metabolic process involving the competition of glucose and fatty acids for substrates.[1] It is theorized to play a role in explaining type 2 diabetes and insulin resistance.[2][3]
The mechanism involves malonyl-CoA and its inhibition of carnitine palmitoyltransferase I (CPT1). Glucose oxidation produces citrate which can be converted to malonyl-CoA by acetyl-CoA carboxylase (ACC1 or ACC).

Malonyl-CoA then can bind to and inhibit one of several tissue-specific CPT1 isoforms. CPT1 is a transporter of long-chain fatty acids at the outer mitochondrial membrane that regulates the rate-controlling step for fatty acid oxidation. Thus, increased glucose oxidation inhibits fatty acid oxidation via malonyl-CoA, which can then be utilized as a substrate for fatty acid synthesis.

It is named for Philip Randle, who described it in 1963.” – Wikipedia
In other words, cells flip back and forth between two different sources of fuel, which can consist of either glucose, or long chain fatty acids. It is a constant flux, but in the presence of large amounts of long chain fatty acids, glucose will be refused entry, and vise versa. What are long chain fatty acids? Well, unsaturated fats are long chain fatty acids, and that includes our favorite polyunsaturated (PUFAs) fats, like the vegetable and seeds oils that have “saturated” our food industry over the last hundred years or so. Since the S.A.D (Standard American Diet) is overly full of PUFAs, many people are living in a near constant state of turning glucose away from entry into their cells, in order to allow the PUFAs to be burned for fuel. In my opinion, it’s easy to see how such a process could easily become the true starting point for insulin resistance…..the real catalyst that starts the house fire if you like.

This whole mechanism is also one of the reasons that fructose has earned such a horrible reputation recently:

Vegetable Oils With Fructose or Alcohol

These toxic foods are particularly dangerous in combination. We discuss this mix of toxins in the book (pp 56-59).
If you feed lab animals high doses of polyunsaturated fat (either omega-6 or omega-3 will do) along with high doses of either fructose or alcohol, then fatty liver disease develops along with metabolic syndrome. Metabolic syndrome is a major risk factor for obesity, and it’s not very difficult to induce obesity on these diets.

Both sugar and vegetable oils are individually risks for obesity:
  • Stephan did a nice post a few years back, “Vegetable Oil and Weight Gain,” discussing a couple of studies showing that both rats and humans get fatter the more polyunsaturated fat they eat.
  • Dr. Richard Johnson and colleagues did a review of the evidence for sugar (fructose) as a cause of obesity in the American Journal of Clinical Nutrition a few years ago. [1]
What the animal studies show us is that when fructose and vegetable oils are consumed together, they multiply each other’s obesity-inducing effects.” – Paul Jaminet, from the Perfect Health Diet Blog
Fructose in combination with PUFA is bad news, but fructose by itself shouldn’t present an issue. However, it seems that PUFAs either by themselves, or in combination with sugars are almost equally bad news for the human body.

What if sugar doesn’t cause diabetes?

What if PUFAs are actually the cause of metabolic syndrome and diabetes? What if sugar was essentially the innocent bystander? Sure, once a person HAS diabetes, sugars becomes a very large part of the problem, but is that the fault of the sugar? I don’t believe so.

PUFAs build up in fat reserves over time, which serves to exacerbate the whole issue, because many diabetic people are also overweight. However if a person completely avoids PUFAs, given enough time, it’s possible that they could systematically replace all of the PUFA stored in fat tissue, with much more friendly saturated fats. Given this reasoning, it seems entirely possible that if a diabetic person were to simultaneously eliminated all PUFAs, and starchy carbohydrates from their diet for a period of several years consistently, they could fundamentally reverse Type II Diabetes……for good. Maybe that’s precisely why so many Paleo Diet practitioners have been able to reverse their diabetes, even though modern medicine doesn’t believe that it is possible to do so without drugs.

I think that PUFAs should be excluded from everyone’s diet. Maybe it would help to turn the tide on diabetes, and also stop everyone from blaming an entire macronutrient category (carbs) for the creation of diabetes. It doesn’t start with carbs, it just ends with carbs.
Check out this article for more info on the dangers and misconceptions of PUFAs.

Hopefully you now understand a little more, why I say that “The Devil is in the PUFA”, because I think that is where he lives.
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Barry Cripps is a Paleo-based, Certified Nutrition and Wellness Consultant, who operates out of Bowling Green, Kentucky.

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Ketogenic Nutrition: Advanced cancer and the ketogenic diet

Ketogenic Nutrition: Advanced cancer and the ketogenic diet

Thursday, August 11, 2011

Advanced cancer and the ketogenic diet

A new pilot trial about cancer-ketogenic diet has recently been published (1). This german group evaluated specifically the feasibility of a KD and its influence on the quality of life of patients with advanced metastatic tumors. The full text is free, so anyone can go and check the details and methodology used. The nutritional intervention was basically an ad libitum KD (<70g/CHO/day), plus extra omega-3 fatty acids. 

Dietary guidelines for the patients were (Table 2):
  1. Avoid all types of bread, cake, processed snacks, sweets, potatoes, pasta,
    rice, polenta, vegetables rich in starch (corn, beans, peas) and cereals.
  2. Be aware of hidden sources of CHO in sugar sweetened drinks, candy,
    chewing gum with sugar, milk and milk products, lunch meat and some
    cheeses as well as in most “low fat” products.
  3. Fruits are rich in CHO, therefore always calculate the amount and select
    those which are low in CHO.
  4. Vegetables are often rich in CHO - but mainly in dietary fiber, therefore
    calculate the usable CHO only.
  5. If possible, prefer cold-water fish and meat from grazing cattle as protein
    sources, because of their preferable fatty acid pattern.
  6. Vegetables and the few fruits allowed should be grown organic
  7. As nibbles, select oil-rich nuts (walnuts, brazil nuts, macadamia nuts) and
    seeds (sunflower), and only occasionally chocolate with very high cacao
    content (min. 85%).
This guidelines look very paleoish to me (whatever that means). Some things I found interesting are points 5 and 6. Not seen emphasized commonly. Additionally, patients were told to drink two liquid meals as snacks. Components of this shake were provided to the patients and included: 250ml of highly fermented yogurt-drink, 8ml vegetable oil mixture and 10g of protein preparation. Ingredients of the components can be seen in Table 3. 

Because of problems with compliance to the diet, from 16 initial participants, only 5 remained until the end of the study (31%). Two patients dropped out during the first week, one because of inability to adhere to the diet and the other because of personal problems. Two patients died from their malignant disease during the study, one patient dropped out because he suffered excessive weight loss and weakness, one patient quit because he felt he wasnt able to stick to the dietary guidelines, one because resuming chemotherapy and four due to progress of their advanced cancer situation. The compliance problem is common. Adopting a ketogenic diet involves a lifestyle change. Something even advanced cancer patients can't do. This reminds me of a study in which some cancer patients wouldnt adopt a KD because that meant "giving up the candies and ice cream", despite the fact that it could improve their condition. To complicate things further, the acceptance of the diet varied greatly. One patient said that after 3 days on the diet it was not feasible at all and stopped the diet. Two patients rate feasibility as "very good", seven patients rate it "good", three "moderate" and one "poor". This was after 2 weeks of dieting so included the 16 initial participants.

Quality of life was measured by the EORTC QLQ-C30 questionnaire. Global scores remained relatively stable during the evaluation time. Physical and role functioning worsened slightly over time and constipation was reported by most patients. Because of the advanced cancer stage of the patients, fatigue, pain or dyspnoea increased over time. Nevertheless, emotional functioning increased slightly and insomina improved. 

Of those who completed the whole 12 weeks of dieting, 60% reached a stable ketonuria, predominantly being 1.5-4.0mM. Among blood parameters, only some patients had available data. Overall, CRP levels increased slighlty over time, considering the initial values were high. Two patients initially had elevated glucose, which returned to normal. In other patients, cholesterol levels were "normalized" (meant by reduced to conventionally accepted levels), as well as triglycerides in one patient and ALT in other patient. Total leukocyte count significantly increased during the intervention (even though one patient with initial low leukocyte counts showed a further reduction). 

Patients lost an average of 2kg. Progress of the disease occured in 5 patients who then discontinued the diet, while 5 patients who adhered to the diet had stable disease progression.

Overall, the percentage of days in ketosis (>0.5mmol/l) was not correlated with the results of the study. We can see in table 4 that for example, patient 6 reached 97% of days in ketosis, but because of impaired food intake only completed 6 weeks and showed progress in the disease. On the other hand, patient 16 reached 100% days in ketosis, completed the trial and showed no progress in the disease. Both patients 5 and 11 only reached 25% of days in ketosis, but completed the trial and maintained their condition. 

The limitations of this study were:

- Patients had advanced stage cancer. While a KD might help preventing and/or treating some cancers, there is no much left to do when the disease is too severe.

- Most patients werent from the author's hospital. Blood samples and laboratory parameters had to be provided by their family doctors or local oncologists.

- Short sample and short intervention time. 

Being fair, at the time the study was done (2007) guidelines to apply a KD for cancer treatment were scarce. The only premise was that reducing carbohydrates (hence sugar and cancer's fuel) would reduce progression of tumors. Since then, there is more information available which suggest how to implement the KD for these patients. Overall, evidence suggest that the diet should be not only ketogenic, but calorie restricted. This is for achieving low blood glucose levels and increased KB. In the study reviewed in this post, calories were ad libitum and with a carbohydrate intake limited to 70g/day. Glucose should be ideally around 55-65mg/dl and KB 4-7mM. Checking the study data, most patients had much higer BG (mean 93) and only mild ketosis. Therapeutic fasting is another valuable tool, but harder to comply with. Another factor to take into account is the cancer phenotype. A restricted KD should be more efficient in predominantely glucose-consuming tumors, which can be assessed using some phenotypic markers. Serum LDH levels, for instance, have been shown to be correlated with activation of HIF related genes (2), which include glycolytic enzymes (3). Or using the more conventional FDG-PET. Finally, utilization of gluconeogenesis and glycolysis inhibitors (ie. 2-Deoxyglucose or metformin) with the KD has also been proposed (4,5).

Recent evidence suggests that this metabolic therapy is promising. One case report (6) has shown a rapid regression of glioblastoma multiforme in an old patient using the guidelines proposed by Seyfried et al (7). This patient started the metabolic therapy with a water-only fast, switching then to a restricted KD which delivered 600kcal/day for 14 days. Dexamethasone was also eliminated (because high dosage steroid medication increases gluconeogenesis and blood glucose levels, while enhancing apoptosis resistance in tumor cells). Because of development of mild hiperuricemia, the KD was changed for a non-ketogenic calorie-restricted diet which also delivered 600kcal/day. Aside from the complete regression in such a short time (2-2.5 months), the most surprising finding in my opinion was the recurrence of the tumor after discontinuing the metabolic therapy, which strongly suggests that the therapy itself was the most infulential factor in cancer regression.

It seems that controlling blood glucose levels is the more important part of the metabolic therapy. Achieving blood glucose levels of 55-65mg/dl and 4-7mM of ketone bodies has been termed as "the zone of metabolic management":

This resembles the results from the study on the GB patient:

Although target blood glucose levels were not achieved, the reduction observed was sufficient for controlling disease progression. The other difference was the method of detection of ketosis, urinary ketones, which doesnt always correlate to blood ketone levels. 

ResearchBlogging.orgSchmidt M, Pfetzer N, Schwab M, Strauss I, & Kammerer U (2011). Effects of a ketogenic diet on the quality of life in 16 patients with advanced cancer: A pilot trial. Nutrition & metabolism, 8 (1) PMID: 21794124

Is Fish Oil Really Any Better Than Vegetable Oil? - Paleo Diet

Paleo Diet: Is Fish Oil Really Any Better Than Vegetable Oil? » Your source for Paleo Diet information

I’ve found that after residing in the Paleosphere for a few years, there are very few things that I’m able to take at face value anymore. I find that instead of just blindly accepting what someone tells me, I ask lots of questions, and do a substantial amount of my own research BEFORE I will subscribe to an idea. I’m not really sure that any one person out there has all of the answers to this whole nutrition thing. Some people hold several pieces of the pie, while others hold NONE…..although those poor shmucks often think that they know everything, and make a whole lot of noise trying to prove that to the world.

One of the most pervasive beliefs within the Paleo diet (and even within the mainstream), right now is that fish oil is good for us. The had me hook, line, and sinker for a while (pun intended), but the more I think about it, the less convincing the idea is to me. Lately I’ve been asking myself the question, “Is fish oil really any better than vegetable oil?”.

Actual health benefits aside, let’s first talk about the literal “Paleo perspective” on such things. What do we try to do on Paleo? We try to eat whole, real, unprocessed foods to get the nutrients we need, right? So if a Paleo practitioner wants to ensure that they are getting enough EPA, and DHA, should we immediately reach for a bottle of processed oil that was mechanically removed from some un-seen seafood source (we hope it’s really fish!), and bottled by some person that we’ve also never seen……or, should we just eat more fish?
The obvious answer is to just eat more fish…..but I’m not convinced that omega-3 Fatty Acids are as important to us as the mainstream would have us believe. The term “essential” officially means:
“a substance that is not synthesized by the body in a quantity sufficient for normal health and growth and that must be obtained from the diet” – Webster’s Dictionary
So we know that we have to get omega fatty acids from our diet, but there is no RDA (Recommended Daily Allowance) established for them, and no one really even started paying attention to them until the 1970s.
“The health benefits of the long-chain omega-3 fatty acids — DHA and EPA omega-3 — are the best known. These benefits were discovered in the 1970s by researchers studying the Greenland Inuit Tribe. The Greenland Inuit people consumed large amounts of fat from meat, but displayed virtually no cardiovascular disease. The high level of omega-3 fatty acids consumed by the Inuit reduced triglycerides, heart rate, blood pressure, and atherosclerosis.” – Wikipedia.org
The fact that the Inuit people are (were) so healthy, probably can’t be completely attributed to omega-3 fatty acids, considering that they have little to no detrimental environmental factors (except for the extreme cold), no grain consumption, and none of the modern stresses that we deal with today. The FDA obviously isn’t buying the supposed benefits either:
“On September 8, 2004, the U.S. Food and Drug Administration gave “qualified health claim” status to EPA and DHA n−3 fatty acids, stating that “supportive but not conclusive research shows that consumption of EPA and DHA [n−3] fatty acids may reduce the risk of coronary heart disease.”[7] This updated and modified their health risk advice letter of 2001 (see below). As of this writing, regulatory agencies[who?] do not accept that there is sufficient evidence for any of the suggested benefits of DHA and EPA other than for cardiovascular health, and further claims should be treated with caution” – Wikipedia.org
The thing is that fish oil is a polyunsaturated fat. It’s unsaturated, which means that unlike saturated fats, it is liquid at low temperatures, and room temperature. It also means that it is highly unstable, and prone to perioxidation when it is exposed to the air, or to warm temperatures. On the other hand, saturated fats remain solid at room temperature, and don’t go rancid like the unsaturated fats do. When a fat goes rancid inside the body, it causes oxidative damage. It is already established that arterial plaque, is composed of oxidized polyunsaturated fats. See an article about that here. So why do we believe that supplementing with such oils is good? Many of the commercially available fish oil supplements are already rancid when we buy them!

Dr. Ray Peat has some very poignant things to say about fish oil and its effects on human health, in his article entitled “The Great Fish Oil Experiment”:
“In experiments that last just a few weeks or months, there may not be time for cancers to develop, and on that time scale, the immunosuppressive and antiinflammatory effects of oxidized fish oil might seem beneficial. For a few decades, x-ray treatments were used to relieve inflammatory conditions, and most of the doctors who promoted the treatment were able to retire before their patients began suffering the fatal effects of atrophy, fibrosis, and cancer. (But a few people are still advocating x-ray therapy for inflammatory diseases, e.g., Hildebrandt, et al., 2003.) The fish oil fad is now just as old as the x-ray fad was at its peak of popularity, and if its antiinflammatory actions involve the same mechanisms as the antiinflammatory immunosuppressive x-ray treatments, then we can expect to see another epidemic of fibrotic conditions and cancer in about 15 to 20 years.”
“The most popular way of arguing that fish oil will prevent heart disease is to show that it lowers blood lipids, continuing the old approach of the American Heart Association’s “heart protective diet.” Unfortunately for that argument, it’s now known that the triglycerides in the blood are decreased because of the fish oil’s toxic effects on the liver (Hagve and Christophersen, 1988; Ritskes-Hoitinga, et al., 1998). In experiments with rats, EPA and DHA lowered blood lipids only when given to rats that had been fed, in which case the fats were incorporated into tissues, and suppressed mitochondrial respiration (Osmundsen, et al., 1998).”
“Another way of arguing for the use of fish oil or other omega-3 fats is to show a correlation between disease and a decreased amount of EPA, DHA, or arachidonic acid in the tissues, and to say “these oils are deficient, the disease is caused by a deficiency of essential fatty acids.” Those oils are extremely susceptible to oxidation, so they tend to spontaneously disappear in response to tissue injury, cellular excitation, the increased energy demands of stress, exposure to toxins or ionizing radiation, or even exposure to light. That spontaneous oxidation is what made them useful as varnish or paint medium. But it is what makes them sensitize the tissues to injury. Their “deficiency” in the tissues frequently corresponds to the intensity of oxidative stress and lipid peroxidation; it is usually their presence, rather than their deficiency, that created the disposition for the disease.”
”One of the earliest harmful effects of polyunsaturated fatty acids, PUFA, to be observed was their acceleration of the formation of lipofuscin or ceroid, the “age pigment,” during oxidative stress or vitamin E deficiency. Associated with the formation of lipofuscin, the PUFA were discovered to cause degeneration of the gonads and brain, and the fact that vitamin E could prevent some of their toxic effects led to the idea that vitamin E was essentially an antioxidant. Unfortunately, the protective effect of vitamin E against the PUFA is only partial (Allard, et al., 1997).”

“When animals are fed fish oil and then exposed to bacteria, their immunosuppressed thymic (T) cells cause them to succumb to the infection more easily than animals fed coconut oil or a fat free diet. Natural killer cells, which eliminate cancer cells and virus infected cells, are decreased after eating fish oil, and T suppressor cells are often increased. More subtle interference with immunity is produced by the actions of PUFA on the “immune synapse,” a contact between cells that permits the transmission of immunological information. The immunosuppressive effect of fish oil is recognized as a useful aid in preventing the rejection of transplanted organs, but some studies are showing that survival a year after transplantation isn’t improved.”
The statements that Ray makes (above) about fish oil suppressing the immune system, are backed by studies here and here and here….also check this one out.

So, is Fish Oil really any better than vegetable oil? I don’t think so. Personally, I think that we’re all better off, getting the small amount of omega-3 fatty acids that we MIGHT ACTUALLY NEED (which is completely debatable), by eating grass-fed beef. Sure, the non-fatty fish might be a great source of protein, but I just don’t see a benefit to supplementing with fish oil, or going out of our way to eat lots of oily fish. Just eat real food, and increase your saturated fat intake using some lovely, stable, coconut oil!

This is a pretty controversial topic! What do you think? Are we better off NOT taking fish oil? Please leave your comments and observations below in the comments section. And if you found this article interesting, please share on Facebook and Twitter. Join the Paleo Diet News discussion!


Anti-Inflammatory Diet: How to Choose the Right Cooking Oil | The Conscious Life

Anti-Inflammatory Diet: How to Choose the Right Cooking Oil | The Conscious Life

Check out this essential buying guide before getting your next bottle of cooking oil

Cooking oil is a basic and almost indispensable ingredient in every kitchen. But nowadays, there are so many different types of cooking oil that you can literally take an hour or more just to go through all the options in a well-stocked supermarket.
From the ubiquitous refined soybean and corn oils that seem to be in every manufactured food, to exotic and premium oils such as extra virgin avocado and coconut oils.

Which one should you use?

To answer this question, let us put these cooking oils side-by-side and look at their vital statistics. We’ll also discuss what are the things to look for in an edible oil and lastly, go through some oils that fit the bill.



SFA: Saturated fatty acids
MUFA: Monounsaturated fatty acids
PUFA: Polyunsaturated fatty acids
Ω-3: Omega-3 fatty acids
Ω-6: Omega-6 fatty acids
Ω-9: Omega-9 fatty acids
Ω-6:3 Ratio: Omega-6 to omega-3 ratio

Smoke Point:
The temperature at which a cooking oil starts to burn and produce chemicals that are potentially harmful.

How to Choose Your Next Cooking Oil

So what should you look out for in the table full of numbers? Here are some suggestions:
  1. Keep omega-6 and omega-3 intake in balance
    Omega-6 and omega-3 fatty acids contain essential polyunsaturated fatty acids (PUFA) that are important for good health. Our body cannot produce some of these fats, and thus we need to consume them through foods every day.

    … some omega-6 fatty acids tend to promote inflammation, while omega-3 fatty acids help to reduce inflammation.However, the consumption of omega-3 and omega-6 fats needs to be in balance as some omega-6 fatty acids tend to promote inflammation, while omega-3 fatty acids help to reduce inflammation. Some researchers suggest maintaining an omega-6 to omega-3 ratio of 2:1 to 4:1 in one’s diet for general health.
    To make things even more interesting, both omega fats compete for the same enzymes in the body. Having more of one type of omega fatty acids will rob the other of chances to carry out their functions. As a result, the omega-6 to omega-3 ratio in your diet may influence how much pro- and anti-inflammatory compounds are produced in your body.

    Having more pro-inflammatory chemicals than you actually need for prolonged period of time can lead to silent inflammation, which in turn is a malignant seed for many chronic diseases such as diabetes, arthritis, stroke, dementia and some cancers.

    Our modern diet, unfortunately, tends to be loaded with too much omega-6 fats due to the prevalent use of PUFA-rich vegetable oils and inadequate consumption of omega-3, with an estimated ratio of 10:1 to 20:1.

    Combine this a processed food culture and a sedentary lifestyle and you get a global epidemic of chronic disease that we’re seeing today.

    So rather than stoking the flames of inflammation with more omega-6 fats from your cooking oil, go instead for oils with low omega-6 to omega-3 ratio to cut down on your omega-6 intake.

  2. Look out for monounsaturated fats

    Several studies (including this one) suggest that regular use of oil rich in monounsaturated fats such as olive oil may help to reduce the risk of cardiovascular disease by raising HDL (high density lipoprotein), lowering triglycerides and reducing levels of LDL (low density lipoprotein).

    Oleic acid is a monounsaturated omega-9 fatty acid believed to be responsible for the heart-protective effect of olive oil. It is also found in other vegetable and animal oils in varying proportions.

    Further, the phytochemicals in olive oil, for example, hydroxytyrosol and oleuropein, are also believed to play a role in keeping the heart healthy.

    It’s then not too far-fetched to reason that edible oils that have not been overly processed, and so retain more of their phytonutrients, would be a better choice over highly refined and high temperature-treated ones.

  3. Minimize use of oils with high polyunsaturated fats

    Oils containing mostly polyunsaturated fatty acids (50% and above) tend to be unstable and turn rancid more readily than those with high saturated or monounsaturated fats. This is due to the inherent instability of this type of fat molecules.

    The oxidation of polyunsaturated fatty acids (PUFA) begins the moment the oil is extracted and exposed to heat, air and light, breaking down the integrity of the oil and forming free radicals in the process.

    The degradation gets worse when the oil is heated. The higher the temperature, the more inflammatory oxidation products are formed. Hence, you should never heat unrefined, extra virgin PUFA.

    Having said these, it doesn’t mean that you should avoid PUFA-rich oils entirely. Some of these oils, such as flaxseed oil, are excellent sources of plant-based omega-3 fatty acids.

    But, since they break down rather easily, it’s advisable to get such oils as fresh as possible and then to finish them as quickly as you can. They should also always be kept in dark bottles and in the refrigerator to slow down their rate of oxidation.

  4. Choose the right oil for your cooking

    Every oil, no matter how good it may be, will burn when you heat it up long enough. And when oil burns, it rapidly denatures and produces new and potentially carcinogenic compounds.

    … match the right oil with the cooking method you intend to use.Therefore, it’s important to match the right oil with the cooking method you intend to use.

    For instance, if you plan to do stir frying, searing, high-heat baking or roasting, then it’s imperative to choose a cooking oil that can withstand the high heat without disintegrating too much.

    That’s where the smoke point column in the table comes in useful.

    As a general rule of thumb, cooking oils with low smoke point should not be used for high temperature cooking. You can use them for steaming, blanching, stewing in slow cooker, as well as in cold dishes.

    Note that, generally, for the same type of oil, the more refined it is, the higher its smoke point. But bear in mind that that also means the oil would have gone through substantial processing which may have removed most of its beneficial components.

  5. Don’t be afraid of saturated fats

    We’ve always been told not to go near saturated fat if we don’t want to die of a heart attack.

    But in recent years, an increasing number of people are doing just the opposite. Not only are they eating more saturated fats, they are also encouraging others to do so.

    Are they nuts?

    Well, it turns out that there may be some basis to their seemingly suicidal choice.

    Increasingly, more researchers and health practitioners are voicing against mainstream ‘wisdom’ that portrays saturate fat as a artery-clogging and heart-stopping villain.

    They cite ground-breaking studies that failed to find a convincing link associating dietary saturated fats with coronary heart disease (CHD) or cardiovascular disease (CVD) as the reasons.

    Take for instance the literature review supported by the Heart and Stroke Foundation of Canada in 2009.

    In the systematic review of prospective cohort studies and randomized trials from 1950 through June 2007, the authors concluded that there was “insufficient evidence of association” between intake of saturated fatty acids and CHD.

    Instead, they found strong evidence linking regular consumption of vegetables, nuts and a Mediterranean diet (which includes monounsaturated fatty acids) to lower CHD risk, while trans fats and foods with a high glycemic index/load were associated with a higher risk.

    … “no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.”Another meta-analysis of 21 studies published on the American Journal of Clinical Nutrition in 2010 also found “no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.”

    If you’ve always thought that a heart healthy diet is one that contains no animal fats, no butter, no cheese, no coconut milk and certainly no red meat, these brave ‘new’ ideas could come as a shock.

    Have we been blaming the wrong guy all these years?

    Although these studies could not give us a definitive answer, what we can derived from them is perhaps this:

    Like other chronic degenerative illnesses that take years to form, the cause of heart disease is likely to be a combination of many factors, rather than the work of a singular component.

    One’s genetic make-up, physical activity level, personality (which affects one’s susceptibility to stress and his ability to manage stress), family history, place of living, the types of microbe in your gut, and of course, other foods that you eat could affect the outcome of the delicate and complex health equation.

    While the verdict is still out on saturated fat, there’s perhaps no need to avoid saturated fat like the way we used to if you’re generally healthy.

  6. Consider how the oil is extracted

    Industrial refined vegetable oils like soybean and corn oils are usually extracted using toxic chemical solvents such as hexane to pull out more oil from the crops. But inevitably, trace amounts of chemical residue are left in the oil even though steps have been taken to remove them.

    While short term ingestion of small amount of the chemical is unlikely to cause any problems in healthy individuals, long term ingestion is currently unknown. No human study has been carried out so far to assess the long term effects of chronic low-grade exposure to chemical solvent in cooking oil.

    But considering the ubiquitous presence of cooking oil in almost every food we eat each day, do you want to take the chance?

    If you don’t, then you may want to opt for food grade oils that have been extracted mechanically. Such oils are usually labeled as ‘cold-pressed’ or ‘expeller-pressed’. However, because mechanical extraction gives lower yields, oils that are extracted using this method usually cost more.

Recommended Cooking Oils

Considering the factors we have discussed earlier, here are some cooking oils from the list worth highlighting:

Extra Virgin Olive Oil

  • Olives
    Mention monounsaturated fatty acids (MUFA) and most people will think of olive oil. Indeed, more than 70% of fats in olive oil are MUFA, making it the de facto choice for healthful oil.

    As there are many varieties of olive oil, look for reputable organic, cold-pressed extra virgin olive oil. Not only will extra virgin olive oil contain more phytochemicals with potent antioxidant properties, the flavor will also be stronger and richer.

    Vital Fat Composition:

    Omega-6 to omega-3 ratio: 12.8:1
    Omega-3 fatty acids: 0.8%
    Omega-6 fatty acids: 9.8%
    Omega-9 fatty acids: 71.3%
    Saturated fatty acids: 13.8%
    Smoke point: 375°F (191°C) (extra virgin)

    Pros: High levels of beneficial monounsaturated omega-9 fatty acids and an unique flavor.

    Cons: Olive oil’s relatively low smoke point make it unsuitable for high temperature cooking. In fact, you should preferably not cook with extra virgin olive oil. Use it on cold dishes or add it only after you’ve turn off the fire. Further, its distinctive flavor may not be welcomed in dishes that do not call for a taste of Mediterranean.


  • Ghee
    is a type of clarified butter commonly used in India and other parts of South Asia. It shares a similar fat composition as anhydrous butter oil and has an outstanding omega-6 to omega-3 ratio. With a high saturated fat content, ghee does not oxidize easily and has a high smoke point. Although it’s derived from milk, it contains very low lactose and is suitable even for people who are lactose-intolerant.

    Vital Fat Composition:

    Omega-6 to omega-3 ratio: 1.6:1
    Omega-3 fatty acids: 1.5%
    Omega-6 fatty acids: 2.3%
    Omega-9 fatty acids: 25.2%
    Saturated fatty acids: 62.3%
    Smoke point: 485°F (252°C)

    Pros: Rich buttery taste and aroma, excellent omega-6 to omega-3 fatty acids ratio, low polyunsaturated fats, stable and does not oxidize easily, and high smoke point. Suitable for high-temperature cooking.

    Cons: As the health impact of saturated fats is still open to debate, consumption of oils containing high saturated fats should be moderated.

Avocado Oil

  • Avocado
    Avocado oil
    is pressed from the pulp of the avocado fruit, not its seed. It has the highest smoke point among all the cooking oils featured here. Avocado oil is described to have “an aroma of globe artichokes and celery” and “a full rich, lingering flavor of avocado.” Its fat composition is comparable to that of olive oil, containing high monounsaturated fats and acceptable levels of polyunsaturated fatty acids.

    Vital Fat Composition:

    Omega-6 to omega-3 ratio: 13.1:1
    Omega-3 fatty acids: 1%
    Omega-6 fatty acids: 12.5%
    Omega-9 fatty acids: 67.9%
    Saturated fatty acids: 11.6%
    Smoke point: 520°F (271°C)

    Pros: High monounsaturated omega-9 fatty acids. Contains high phytosterols and polyhydroxylated fatty alcohols which are anti-inflammatory in nature. High smoke point also makes avocado oil suitable for high temperature cooking such as stir frying and high heat baking. It’s also reportedly high in vitamin E.

    Cons: Avocado oil is still not as common as other oils. Thus, its rarity may translate into higher cost.

Macadamia Oil

  • Macadamia Nuts
    Macadamia oil
    is extracted from the nut meat of macadamia tree, a native Australian nut. Unbeknown to many people, macadamia oil has even higher amounts (about 12% more) of monounsaturated fatty acids than olive oil. Its roughly one to one ratio of omega-6 to omega-3 fats also made it attractive to people looking to cut down on their omega-6 intake.

    Unlike olive oil which has a stronger flavor, macadamia oil is rather bland and does not carry any strong odor. Due to its relatively high smoke point, it’s also a versatile oil that can be used for different methods of cooking.

    Vital Fat Composition:

    Omega-6 to omega-3 ratio: 1:1
    Omega-3 fatty acids: 2%
    Omega-6 fatty acids: 2%
    Omega-9 fatty acids: 83%
    Saturated fatty acids: 12.5%
    Smoke point: 413°F (210°C)

    Pros: High monounsaturated omega-9 fatty acids, excellent omega-6 to omega-3 fat profile, low polyunsaturated fats, taste that does not overpower other food, and relatively high smoke point. Suitable for stir-fries, baking and pan frying.

    Cons: May not be a good choice for cold dishes, such as salad, that need added flavor from the oil.



Coconut Oil

  • Coconut
    About 50% of the fats in coconut oil are lauric acids, a type of saturated fatty acid that has antibacterial, antioxidant and antiviral properties.

    According to a preliminary study, consumption of lauric acid may increase total cholesterol level with most of the increase being HDL, the ‘good’ cholesterol.

    So rather than increasing the risk of cardiovascular events, lauric acid-rich oils such as coconut oil may confer heart-protective effects instead.

    The high saturated fat contents of coconut oil also made this aromatic oil very stable and resistant to rancidity. At 76°F (24°C) and above, coconut oil is a transparent liquid, while at lower temperature, it solidifies into a hard white mass. You can store coconut oil without refrigeration for up to two years, though I’d recommend that you consume any oil that you buy as quickly as possible while it’s still fresh.

    Another interesting feature of coconut oil is that it contains high levels (about 66%) of medium chain triglycerides (MCTs).

    Unlike long-chain fatty acids, MCTs do not need bile salts for digestion and are easily absorbed and utilized by the body. That’s why MCTs are used clinically in the treatment of malnutrition or malabsorption syndromes.

    Vital Fat Composition:

    Omega-6 to omega-3 ratio: Not a source of omega-3 fatty acids
    Omega-3 fatty acids: 0%
    Omega-6 fatty acids: 1.8%
    Omega-9 fatty acids: 5.8%
    Saturated fatty acids: 86.5%
    Smoke point: 350°F (177°C) (extra virgin)

    Pros: Virgin coconut oil imparts a fresh coconut flavor, is low in polyunsaturated fats, does not turn rancid easily, and a good source of lauric acids. Coconut oil’s antibacterial and antioxidant properties also make it an outstanding choice for luxurious massages.

    Cons: Negligible omega-3 fats content. The distinctive taste and odor of coconut oil can also overwhelm foods that do not have a strong flavor. Virgin coconut oil does not have a high smoke point. Its high levels of MCTs may also make the oil unsuitable for people with liver problems.

    As the health impact of saturated fats is still open to debate, consumption of oils containing high saturated fats should be moderated.

  • Most figures in the table are computed using data available from the USDA database. Smoke point values are retrieved from Wikipedia, as well as the book, The Hamptons Diet.

  • The values here are only meant as a guide. Fatty acids composition of oils differ from brand to brand as well as the country of production.

Why Canola Oil is Not in the Recommended List?

Some sharp-eyed readers have written to ask why canola oil is not in the list of recommended cooking oil. After all, its excellent omega-6 to omega-3 ratio, low saturated fats and high monounsaturated fat levels made it an attractive option. However, as it turns out, canola oil may be no better than industrial refined vegetable oils like soybean oil. Here are the reasons why:
  • Genetically modified source. Canola oil comes from certain types of rapeseed that have been bred using traditional methods to lower its glucosinolate content. (Glucosinolate, by the way, is toxic in high quantity.) This is fine and well until genetically modified rapeseed was developed to make the crop more resistant to herbicide. Now, it’s estimated that some 80% of canola plants in the US and Canada are either genetically modified (GM) or have been contaminated by GM crop.

  • Hexane extracted. Bulk industrial canola oil is usually extracted with hexane, a chemical derived from crude oil, like many soybean and corn oils. Hexane gas is classified as a hazardous air pollutant by the US Environmental Protection Agency because of its health-impairing properties. While the amount of hexane residue in canola oil is small and is unlikely to cause any ill effects when used for short period of time and in small quantity, chronic long-term exposure to hexane residue is unknown. There are canola oils that are expeller pressed, not hexane extracted, but they represent only a small percentage in the consumer market due to lower yield and higher cost of the extraction method.

  • Unstable oil. Canola oil contains relatively high levels of polyunsaturated fatty acids which makes it more prone to oxidation. Unless steps are taken to slow down the oxidation, freshly extracted canola oil degrades quickly, producing a foul smell in the process. To make the final product more appealing to consumers, the bad smell is removed by manufacturers during the oil refining process.
Whether or not highly refined GM canola oil is safe for consumption is a contentious issue fiercely debated by many people (including those involved in the canola oil supply chain). If you’re interested, I encourage you to read the discussions available on the Web and then come out with your own conclusion.

Having said all these, there is no reason why you shouldn’t use a good organic, non-GM, cold-pressed and nitrogen-sealed canola oil from a reputable source.

Final note: No matter how healthy a cooking oil may be, bear in mind that it’s still high in calorie. Over-zealous use of oil can cause unwanted weight gain and lead to obesity.