Monthly Archives: July 2012


Hey Journey Fans!!! Please Please head over to my new website for my blog!!! This one will eventually be shut down as I have finally gotten my site up with hosting capabilities from brain host, and it allows me to add much more content to it for you to enjoy. Lots of the latest paleo resources just a click away and it all helps support the efforts of me bringing info to you!! I’m working through the bugs, and the layout, but all the info from this blog is there.  Thank you all for your support and continued success to you in your own journey!!

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QUESTION EVERYTHING YOU HAVE BEEN TAUGHT – A Registered Dietician’s Letter to the ADA

Journey fans, you are in for an amazing post.  There are far more intelligent folks than I out there doing countless hours of research and questioning everything we have been taught, and when I happen to come across them in my interactions, I am in awe with their knowledge and wisdom they share so freely.  What you are about to read is some of the best research and challenges to a system of lies you will see in one post (In my opinion).

I was browsing around in one of my groups and came across a note posted by a friend, and I was absolutely blown away at the amount of research this amazing woman did to challenge the system of bogus information that has been purported to us since the “lipid hypothesis” has been pushed on us.  Most everyone who has adopted a real food/ancestral eating approach has known about the lies of conventional wisdom, and have read several of these studies at different times, but never have I seen so much research in one single post countering the conventional system.  This amount of info may be lost on some, but if you at all care about your health, and wish to see what true research can lead to, please read, digest and share this post so that everyone can learn the truth!!

I want to thank you Annette Presley for your bravery in challenging the system of lies, for allowing your amazing letter and research to be shared, and for your dedication to the health of us all!!


The paper I sent to the American Dietetic Association

By Annette Hunsberger Presley in Healthy Nation Coalition

Thank you for this opportunity to delve into the science behind hyperlipidemia and its effect on health.  The advice we give the American public will affect their longevity and quality of life and, therefore, I believe we need to be diligent in seeking the facts about cholesterol, saturated fat, and heart disease so that our advice reflects the most up-to-date and accurate science.

From the Evidence Analysis Library, I was able to obtain the following facts: 1) Saturated fat raises both LDL and HDL so it appears not to have a deleterious effect on the Total cholesterol/HDL ratio; 2) There is no evidence to support or not support a high carbohydrate diet or a high fat diet in the treatment of elevated triglycerides; 3) Polyunsaturated fats lower LDL cholesterol; 4) Fiber lowers LDL cholesterol; 5) Omega-3 fats lower LDL cholesterol; and 6) Trans fat raise both LDL and HDL and is, therefore, worse than saturated fat in its effects on cholesterol.

(NOTE there is a typo in this first paragraph.  Annette has corrected this and the response from the comments is here)

The Evidence Analysis Library (EAL) is a compilation of research available to members of the American Dietetic Association (now called the Academy of Nutrition and Dietetics (AND). The AND found me guilty of violating 3 ethics and asked me to do an educational intervention. I was supposed to go on the EAL, research LDL cholesterol and explain why I was going to go back to recommending vegetable oils instead of animal fats. The EAL does not contain all the research there is, and it is quite obviously biased in it’s interpretations of research, but that is the information I was told to use, so I did, but instead of writing the paper they asked for, I wrote one that demonstrated there was no science to back up our fear of saturated fat and cholesterol.

The facts I got from the EAL, I do not dispute. It is true that fiber and omega-3 fats lower LDL. It is true that saturated fat raises both HDL and LDL and it is true that trans fat raises LDL. What was not available on the EAL is why any of these facts make a difference to our health or why we need to have a cholesterol level under 200 in order to be healthy. There needs to be some evidence that lowering LDL or raising HDL prevents disease and evidence that shows a relationship between cholesterol levels and disease. None of that ‘evidence’ was available on the EAL.

Yes, that is a mistake which was not in my original letter, so I must have done some editing and edited in the wrong place. Sorry for the confusion.

The above facts are all well and good, but I was unable to find any science connecting blood cholesterol levels to heart disease or the lowering of blood cholesterol to the prevention of heart disease.  I also did not find any discussion on the effects of LDL particle size (even though this has been a significant focus in cholesterol research since the 1980s) in the prevention or causation of heart disease.  I think it is essential to have these questions addressed.  After all, why are we trying to lower cholesterol?  We need to have sound science behind the why in order to be truly science-based and in order to be sure that we are giving out the right advice.

Because my questions were not addressed in the Evidence Analysis Library, I also read The Cholesterol Wars: The skeptics vs. the preponderance of evidence by Daniel Steinberg, a supporter of the lipid hypothesis, and The Great Cholesterol Con: Why everything you’ve been told about cholesterol, diet and heart disease is wrong! by Anthony Colpo.  After reading these books, I have a good idea of the beliefs on both sides of the cholesterol question and I believe both sides have some merit.

What is the lipid hypothesis?  According to Daniel Steinberg, the lipid hypothesis “postulates that hypercholesterolemia is a major causative factor in atherosclerosis and coronary heart disease.”  The hypothesis “relates to blood lipids, not dietary lipids, as the putative directly causative factor.”

Others interpret the lipid hypothesis as “saturated fat and cholesterol in the diet raise blood cholesterol levels which leads to atherosclerosis and heart disease.”  There are two factors to consider:  A blood lipid-heart relationship and a diet-heart relationship.  There are actually two different hypotheses, the lipid hypothesis and the diet-heart hypothesis.  What evidence do we have to support either of these two hypotheses?

  1. Autopsy evidence

In 1936, Landé and Sperry autopsied 123 individuals ranging in age from eleven to eighty and wrote, “No relationship was evident, and it is concluded that the incidence and severity of atherosclerosis are not directly affected by the level of cholesterol in the blood serum per se.” (1)

In 1961, an Indian study also showed no correlation between serum cholesterol levels and the amount or severity of atherosclerosis (2).  Autopsies conducted on war veterans in 1963 showed no correlation between serum cholesterol and atherosclerosis and even found that those with blood clots and other features of CHD had lower mean cholesterol levels than those who did not have any CHD features (3).

The 1968 International Atherosclerosis Project examined plaques in the arteries of 22,000 corpses in 14 nations and found that populations in all parts of the world had the same degree of atheroma whether they were meat eaters or vegetarians or whether they suffered a great deal of heart disease or very little to no heart disease (4).

A few studies have claimed a relationship between serum cholesterol and atherosclerosis, but the best correlation coefficient was only 0.36 which is rather weak and certainly would not support any claims of ‘significant’ association (5-8).

Autopsy studies do not appear to support the blood lipid-heart hypothesis, instead pointing to atherosclerosis as a normal, unavoidable process.  Also, the degree of plaque build-up does not appear to be related to the incidence of heart disease.  We cannot prove or disprove a diet-heart relationship with autopsy studies since we do not have adequate data on what these people ate.

  1. Animal evidence

Nikolai Anitschkow (9) fed rabbits a high cholesterol diet and found that they developed atherosclerosis similar to that found in humans, but they also developed plaque in organs and other tissues, unlike humans, probably due to the fact that rabbits are herbivores and do not have any way to process cholesterol.  Feeding cholesterol to rabbits also raises blood cholesterol levels to an astronomically high level not seen in humans.  Studies on other mostly herbivorous animals such as guinea pigs, chickens, goats and parrots also showed plaque build up with cholesterol feeding.

Carnivorous animals, on the other hand, do not respond the same as herbivores to cholesterol feeding.  Dogs can take in a large quantity of cholesterol without developing plaque or high blood cholesterol levels, but they will suffer elevated blood cholesterol levels and atherosclerosis if the thyroid is removed or suppressed with medication (10).  Several studies also showed that rabbits fed high cholesterol diets along with iodine or thyroid gland did not develop atherosclerosis (11, 12).

When rabbits develop atherosclerosis, their plaques never rupture and they don’t get heart attacks like humans.  Many other animals are the same way and it may be due to the fact that rabbits and other animals make their own vitamin C, whereas humans do not.  The balance between collagen degradation and collagen synthesis is one of the main determinants of plaque rupture (13) and vitamin C is essential for the synthesis of collagen.

Animal studies, alone, are unable to prove or disprove anything for humans due to differences in physiology, but, they can provide some data that may be useful to look at in humans.   Animal studies do show that elevated cholesterol levels in the blood produce atherosclerosis, and we also know that people with familial hypercholesterolemia have elevated blood cholesterol levels and a higher rate of heart disease.  What animal studies can’t tell us is what causes the elevated cholesterol in humans, whether it is the mere presence of elevated cholesterol in the blood stream or the combination of elevated cholesterol and some other factor such as iodine or vitamin C deficiency that causes atherosclerosis or whether there is something entirely different going on that may be the cause.

  1. Epidemiological studies:

We have Ancel Key’s Seven Countries Study (14) where he picked seven countries and plotted on a graph mean cholesterol levels for each country and the number of coronary deaths in that country.  He was able to show that Japan, which had the lowest cholesterol levels, also had the lowest rates of coronary death while Finland, with the highest cholesterol levels, had the highest rate of coronary death.  The other five countries fit neatly in a line on this graph.  The rate of coronary death appeared to relate to the level of blood cholesterol.  The countries with higher rates of heart disease also had higher saturated fat intake.

There are several problems with this study.  At the time, data was available for 22 countries and if all 22 countries are put on the graph, there is no correlation between blood cholesterol levels and coronary death.  In fact, if Keys had chosen to use Finland, Israel, Netherlands, Germany, Switzerland, France and Sweden instead of Italy, Greece, Yugoslavia, Netherlands, Finland, USA and Japan, he would have shown the exact opposite effect; the higher the blood cholesterol levels, the lower the incidence of coronary death.  Researchers also found a significant difference in iodine intake between Eastern and Western Finland with no significant difference in saturated fat or cholesterol intake.  Eastern Finland had higher rates of heart disease and lower iodine intake (15).

I don’t believe we can use this study to support the lipid hypothesis or the diet-heart hypothesis as it is so clearly biased and manipulated.  A study like this would never be taken seriously by today’s scientific standards and there is good evidence that it is not blood cholesterol or saturated fat that is the issue.  Inadequate iodine intake is associated with CHD.  The Japanese diet happens to be high in iodine, so is it the iodine that offers protection, the low saturated fat diet, or some other factor?

We also have the Japanese migration studies (16) where the Japanese from native Honshu were compared to Japanese who had migrated to Hawaii and San Francisco.  The results showed higher cholesterol levels in the Japanese from Hawaii and San Francisco as well as higher rates of heart disease.  The assumption is that a higher saturated fat diet was the cause of the elevated cholesterol, but in a follow-up study (17), one of the researchers, Dr. Marmot, found that the Japanese Americans who retained their traditional culture, but ate higher fat American foods were much better protected from heart disease than the Japanese Americans who adopted the American lifestyle but ate the lower fat Japanese diet.

The Japanese migration studies seem to indicate that it is not saturated fat or elevated cholesterol levels, but lack of social ties that increase heart disease risk.  While the Japanese enjoy the longest average life expectancy in the world, they got to that point while increasing saturated fat intake.  Life expectancy in Sweden is only 2 months shy of life expectancy in Japan, yet the Swedes have a high saturated fat intake (18).

Daniel Steinberg claims that The Framingham study “provided the first solid and unarguable evidence that individuals with higher blood cholesterol levels at the time of the baseline examination were more likely to experience a myocardial infarction in the subsequent years of follow-up.”  Researchers found that elevated baseline cholesterol was associated with increased mortality in people under 50, but found no relationship between cholesterol and CVD in those over 50. Researchers also had to admit; “There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years…”  The study found that for every 1mg/dl per year drop in cholesterol levels during the first 14 years, there was a 14% increase in CVD and an 11% increase in overall mortality during the subsequent 18 years (19).  However, this fact was reported as, “a 1% reduction in cholesterol corresponds to a 2% reduction in CHD risk.” (20)

If we look at the facts from Framingham, we find an association between cholesterol levels taken at baseline and myocardial infarction years later in people under 50.  We also find that lowering cholesterol levels increases the risk of all cause mortality and heart disease.  What we don’t know is 1) why a high baseline cholesterol level appears to increase the risk for heart disease as opposed to high cholesterol later on; 2) what other factors were present that might contribute to heart disease; or 3) whether the people with high initial cholesterol died because they tried to lower their cholesterol.  From Framingham, it does not appear that lowering cholesterol is beneficial.

Professor John Yudkin analyzed data from 15 countries and found extreme variations in heart disease and fat intake.  Some countries with high fat intakes had low rates of heart disease, while other countries with identical fat intake had very different rates of heart disease.  Yudkin examined more than dietary fat; he also included fat as a percentage of calories, different types of fat, carbohydrates and protein in his analysis and found that sugar intake showed the strongest association with CHD (21).  Yudkin also found higher rates of CHD in countries with the most TV, radio and car ownership.

The Pukapuka and Tokelau people in the South Pacific have a high saturated fat diet due to coconut intake, but researchers note a complete lack of CVD in these populations despite an average blood cholesterol level of 240 mg/dl in Tokelau (22).

The Masai in Africa live on fat-rich milk, meat and blood with an average intake of 300 grams of animal fat daily.  Professor George Mann found the Masai to be slim and fit and virtually free of heart disease (23) and despite their very high saturated fat intake, most of them had blood cholesterol levels below 160 mg/dl (24).

Of twenty-five prospective studies examining a link between saturated fat and CHD between 1963 and 2005, six (25-30) found an increased risk of CHD with saturated fat intake, though in two of the studies (29, 30), after adjusting for confounders, such as age and smoking, there was no significant association between saturated fat intake and incidence of CHD.  The other nineteen (31-49) studies found no link between CHD and saturated fat.  If we take a close look at the four (25-28) that found a connection, one would increase their risk for heart attack by increasing their saturated fat intake by a mere 0.5 to 1.7 percent of calories.  On a 2000 calorie diet, that amounts to 1.1 to 3.8 grams of saturated fat.  In the Honolulu Heart Program, the difference between saturated fat intake between those who remained free from CHD and those who died of a heart attack was only half of one gram.

I don’t believe we are being scientifically objective if we believe that the microscopic differences in saturated fat intake in a few studies is proof of the lipid hypothesis or the diet-heart hypothesis.  Not only is that quite a stretch to believe, but we would also have to ignore nineteen studies that showed no association between saturated fat and CHD.

Epidemiological studies, of course, cannot prove causation, only association, and many of these studies measured more than one dietary component, so we can’t be sure which dietary component was more significant.  But, the epidemiological evidence does not appear to support either the lipid hypothesis or the diet-heart hypothesis, unless the dietary component is sugar or, perhaps, a lack of iodine or unless we are to believe that 1 to 4 grams of extra saturated fat per day is the difference between life and death.

  1. Dietary Intervention Trials

Out of seventeen trials (50-66) conducted between 1946 and 2006; there are six trials (50, 53, 59, 60, 64, and 65) that found a statistically significant mortality benefit with intervention.

Morrison (50) placed 50 heart attack patients on a low-fat, high protein diet with supplemental calcium, phosphorus, wheat germ and brewer’s yeast (treatment group).  Another 50 patients were on their typical diet (control group).  At the end of the study, thirty-eight patients in the control group had died compared to twenty-two in the treatment group.  The problem here is that multiple interventions were used.  Was it the low-fat diet, the high protein diet, the calcium, or B-vitamin containing brewer’s yeast or a combination of all of them or several of them that were responsible for the results?  We don’t know, so we cannot say with certainty that it was the low-fat diet.

Hood et. al. (53) conducted a non-randomized, non-blinded trial with 460 patients.  The dietary intervention group was put on a low saturated fat, high polyunsaturated fat diet and received close medical supervision whereas the control group was not supervised at all.  The researchers found a significant decrease in total mortality in the intervention group, but the control group had a significantly higher number of high-risk, CHD-prone patients.  This study clearly has some serious flaws.  Was the higher death rate in the control group due to the lack of medical supervision, the diet or the fact that more people prone to CHD were in this group?

The Oslo Diet Heart Study (59) randomized over 400 men to a diet or control group.  The diet group lowered saturated fat and margarine intake and ate a high polyunsaturated fat diet.  They experienced a significant reduction in blood cholesterol, CHD incidence and mortality, so this would appear to support the lipid hypothesis and the diet-heart hypothesis.  However, those in the diet group were also told to increase nut, fruit and vegetable intake which would increase antioxidants and other cardio-protective nutrients.  In addition, the men in the diet group were told to eat more fish and were supplied with sardines canned in cod liver oil.  Fish has been shown to be cardio-protective and cod liver oil contains vitamin D which is now being recognized as an important nutrient for heart health.  The diet group did contain more hypertensive men, but the control group had more overweight men and more men over the age of sixty.  Though both groups started out with the same number of smokers, the control group ended up with significantly more heavy smokers.  I don’t believe we can objectively state that a decrease in saturated fat is responsible for the lowered CHD incidence and mortality.  It could be the sardines in cod liver oil, the increase in nut, fruits or vegetables or the decrease in trans fat.  There are too many variables to single out one as “the” culprit.

The Finnish Heart Study (60) was very poorly designed and received a lot of criticism.  Patients in two different hospitals were studied.  For six years, hospital K received a high polyunsaturated diet and hospital N received their normal diet and then it was reversed.  Patients were included in the study even if they were admitted for a month or if they were discharged and readmitted a year later.  The study was also not randomized or blinded.  A significantly lower number of CHD deaths were found in those on the experimental diet, though in women, it was only significant for those in hospital N.  Because of the poor design, we could hardly use this study as proof positive of the lipid hypothesis or the diet-heart hypothesis.

The STARS trial (64) involved sixty people.  Half were told to lower intake of saturated fat, vegetable oils, margarine and refined carbohydrate-rich junk foods.  They were to limit meat, fish and dairy products and increase fruit, vegetable and complex carbohydrate intake.  The treatment group did have higher DHA levels indicating that not all of them decreased their fish intake as instructed.  At the end of the study, there was 1 death in the treatment group and 3 deaths in the control group and 10 treatment subjects had widening of the arteries compared to only one in the control group.  This study is used to declare decisive proof that saturated fat and trans fat cause coronary occlusion.  Again, the problem is that the treatment diet involved several different variables, so we cannot objectively say that saturated fat was the culprit.  It may have been the decrease in refined carbohydrate or trans fat or the increase in fruit and vegetable intake or a combination of the above.  The prescribed diet, which included lowering saturated fat, worked, but was it because of the lowered saturated fat intake?  We can’t answer that question, scientifically.

The Lion Diet Heart Study (65) randomly assigned 605 recent heart attack patients to one of two groups.  The control group did not receive any specialized dietary instruction other than what may have been given by their physician or hospital dietitian.  Those in the treatment group were advised to eat a Mediterranean type diet with increased vegetables, bread and fish.  Chicken was to replace red meat, olive oil or a high omega-3 fat canola oil based margarine was to replace butter.  Fruit was to be eaten daily.  The study was cut short at twenty-seven months because CHD was slashed by 81% and total mortality by 60% in the treatment group.  However, the differences between the treatment and control group could not be explained by blood cholesterol levels since both groups had identical total cholesterol and LDL-C levels during the entire study.  This study would not support the lipid hypothesis since blood cholesterol levels were the same in both groups.  Nor does it support the diet-heart hypothesis, as once again, there are too many dietary variables to declare with certainty that it was the lowering of saturated fat that caused the favorable results.

Rose et. al. (51) compared the effect of corn oil, olive oil and saturated fat on CHD.  The corn oil group had significantly increased CHD incidents, deaths and total deaths despite the fact that they had a lower blood cholesterol level than the saturated fat group.  The olive oil group didn’t do much better than the corn oil group.  Those in the saturated fat group lived the longest.

The DART trial (63) had three different groups; a group that ate more fish, one that lowered fat intake while increasing the ratio of polyunsaturated to saturated fat and a group that ate more cereal fiber.  They found no mortality change in the low-fat group, a slight increase in mortality in the fiber group and a significantly lowered mortality in the fish group, despite the fact that blood cholesterol levels went up in the fish group.

Recently, the Women’s Health Initiative (66) showed no benefit to lowering total fat or saturated fat in the diet in preventing heart disease.  In fact, those with existing heart disease were at increased risk for events on the lower fat diet.

The Multiple Risk Factor Intervention Trial (MRFIT) (67) tested several variables such as a low fat diet, smoking, exercise and blood pressure on heart disease risk but was unable to find any significant decrease in coronary artery disease.  Steinberg points out that the difference in cholesterol levels between the control and test group was only 2%, so there wasn’t enough cholesterol lowering in the test group to make a difference.  To me, this would indicate that saturated fat and cholesterol intake does not significantly raise blood cholesterol levels and a low fat, low cholesterol diet doesn’t significantly lower blood cholesterol levels and therefore does not support a diet-heart hypothesis.  Since the difference in cholesterol levels was minor, it is possible that lowering cholesterol further may provide protection, so we can’t say with certainty that MRFIT does not support the lipid hypothesis, but MRFIT clearly does not support a diet-heart relationship.

The most widely used study to prove the lipid hypothesis is the Lipid Research Clinics Coronary Primary Prevention Trial (LRCCPPT) (68, 69).  Both the treatment and control groups were put on a low saturated fat and low cholesterol diet and instructed on that diet by a dietitian.  The treatment group also received a cholesterol reducing drug.  The trial participants were all middle aged men with cholesterol levels higher than 95% of the population (they all, most likely, suffered from familial hypercholesterolemia).  The treatment group experienced 19% fewer CHD events than the control group which was barely significant.  Both non-fatal and fatal coronary events had to be added together to get a barely significant finding.  Taken separately, there is no significant difference between the treatment and control groups.  The original design of the study was to use the more stringent significance level of .01 as opposed to the normal .05 because they wanted to make sure there was a real difference.  They ended up using the less stringent .05 level because they could not find any significant differences with the .01 level.  But just for argument sake, lets say this study offers proof of the lipid hypothesis.  What about all the other studies that don’t show any proof and in fact contradict it?  We cannot objectively use one study that shows a barely significant result in people with a genetic defect as proof positive.  This study also does not prove the diet-heart hypothesis since both groups were put on the exact same diet.  We cannot make any objective statements about diet from this study.

In 2006, after examining all the available clinical evidence, Hayward et. al. reported that,”…current clinical evidence does not demonstrate that titrating lipid therapy to achieve proposed low LDL cholesterol levels is beneficial or safe.”(70)

Overall, the dietary intervention trials do not support the diet-heart hypothesis.  There are more studies showing no correlation between saturated fat and cholesterol intake and heart disease than studies showing a correlation and several studies show a health benefit for saturated fat intake. Those that do show a correlation are flawed or contain too many variables to give us any definite answers.  I do not see how we can objectively or scientifically reject the numerous negative studies to support the few positive studies.  The evidence is, at best, extremely weak to support the advice to lower saturated fat and cholesterol in the diet.

The lipid hypothesis is another matter.  I do believe enough evidence exists from the above data and from studying people with familial hypercholesterolemia to look at blood cholesterol a little more thoroughly.  What we don’t know, at this point, is to what extent blood cholesterol matters or if it is solely blood cholesterol or a combination of factors that present health problems.  So far, simply lowering blood cholesterol levels has not produced significant results across the board, so maybe we need to do something in addition to lowering cholesterol, or something else entirely.

We know that people with familial hypercholesterolemia have higher rates of heart disease.  We also now know that they have a defective LDL receptor gene so that they have difficulty getting cholesterol from the blood into the cells.  That is why they have higher than average blood cholesterol levels.

Statin trials have shown that coronary events are reduced even if LDL is not lowered (71-76).  In the PROSPER trial, those with the highest LDL cholesterol levels lived the longest (77).  In the Japanese Lipid Intervention Trial, the highest death rate was seen among those with cholesterol levels below 160 mg/dl.  The lowest overall mortality rate was seen in those who had blood cholesterol levels between 200-259 mg/dl and LDL between 120-159 mg/dl.  In humans, 20 mg/day for 9 days of atorvastatin administration reduced oxidized LDL, but did not reduce blood levels of LDL (78).

Based on the evidence, statins appear to exert a positive effect on CHD through some other mechanism besides cholesterol lowering which would imply that the lipid hypothesis is incorrect in its present form.  It appears that the presence of oxidized LDL is more important than the amount of cholesterol in the blood.  Steinberg also points out very clearly in chapter 5 of his book that it is oxidized LDL that leads to atherosclerosis.  When cholesterol cannot make it into the cells, it has to “wait” in the blood stream.  While “waiting” it is exposed to free radical damage which changes native LDL (large, fluffy particles) into oxidized LDL (small, dense particles).  References 79 through 83 explain the development of and atherogenic properties of oxidized LDL.  What we need to do is find a way to get cholesterol into the cells and a way to prevent LDL from becoming oxidized.

Are there dietary measures we can take to prevent LDL from becoming oxidized?

The component of LDL that is the most likely to become oxidized is the polyunsaturated fatty acids (PUFA).  LDL from people who consume more PUFA from vegetable and fish oils oxidizes more easily and vitamin E does not help to minimize that oxidation (84).  It is the linoleic acid component of oxidized LDL that leads to atherogenesis (85).  A 2004 study by Mozaffarian et. al. showed that postmenopausal women who ate more PUFA, had worsening atherosclerosis over time, but for those who ate more saturated fat, the less their atherosclerosis progressed.  In the highest intake of saturated fat, atherosclerosis actually reversed over time (86). Herron et. al., in 2004, noted that a high cholesterol diet protects LDL from becoming oxidized (87) and yet another study showed egg consumption to be protective of LDL (88).  Milk fat has also been shown to be negatively associated with CVD (89, 90).  Polyunsaturated fats have also been shown to increase cancer risk (91-93) and to play a role in acute respiratory distress syndrome (94).  Antioxidants have been shown to protect LDL from oxidation (95-96).

After all this research, I have come to the conclusion that both proponents and adversaries of the lipid hypothesis have blind spots.  Proponents have recognized the role oxidized LDL plays in atherogenesis and the role the LDL receptor gene plays in getting cholesterol into the cells, but still insist that we should control cholesterol production to reduce the amount in the blood.  They still insist on lowering LDL even though studies show it is not the amount of LDL but the amount of oxidized LDL that is the problem.  They insist on a low saturated fat and cholesterol diet even though they admit that diet does not play a role in the lipid hypothesis. Adversaries of the lipid hypothesis insist that cholesterol does not play a role in heart disease, despite evidence that oxidized LDL promotes atherosclerosis.

It appears to me that we may be doing more harm than good in recommending a diet high in vegetable oils and low in saturated fat and cholesterol.  After all, we developed heart disease, cancer, diabetes and obesity while decreasing saturated fat intake and increasing vegetable oil intake.  It seems ridiculous to blame a fat that has been around for thousands of years for diseases that have only been around for the past 100 years.  Vegetable oils have also only been used in the past 100 years.  The currently accepted low-fat, food-guide-pyramid diet may be causing the very disease we are prescribing the diet to prevent.  Based on the evidence, I cannot with a clear conscious recommend a diet high in vegetable oils and low in saturated fat.  There is just no good science to support that recommendation and a good deal of science that would contradict that recommendation.  I believe it is more important to be scientifically correct than politically correct.  And politics has played a more significant role than science in our dietary recommendations whether we choose to believe that or not.

Dietitians are promoted as “the nutrition expert.”  How can we possibly make that claim if we do not abide by what the science actually says?  How can we claim to be science-based when we ignore every piece of science that contradicts the view we want to take?  Our view should be based on the actual science, not the politics behind the science.  The science that has come out in the last twenty to thirty years clearly contradicts the diet-heart hypothesis and the lipid hypothesis in its present form.  So, trying to lower total cholesterol and LDL cholesterol is a waste of time because it does nothing to prevent LDL from becoming oxidized and, therefore, is not helpful in preventing atherosclerosis.

Based on all the evidence so far, I believe the following:

  1. There is no scientific support for the diet-heart hypothesis, the belief that saturated fat and cholesterol in the diet cause atherosclerosis and heart disease.
  2. The lipid hypothesis is not true in its present form.  It is not the amount of cholesterol in the blood that matters, but the amount of oxidized LDL, so I would support the oxidized lipid hypothesis.
  3. I support diet recommendations that prevent the oxidation of LDL.
    1. Reduction of PUFA intake
    2. Increase in cholesterol and saturated fat intake
    3. Increase in antioxidant intake
  4. I support looking into ways to increase LDL receptor function.  A recent study shows that curcurmin may be beneficial here (97) and thyroid hormone and iodine may play a role as well.




  1. Lande K. E., Sperry W. M.  Human atherosclerosis in relation to the cholesterol content of the blood.  Archives of pathology, 1936; 22: 301-312.
  2. Mathur KS, et al.  Serum cholesterol and atherosclerosis in man.  Circulation, 1961; 23; 847-852.
  3. Paterson JC, et al.  Serum lipid levels and the severity of coronary and cerebral atherosclerosis in adequately nourished men, 60 to 69 years of age.  Circulation, 1963, 27; 229-236.
  4. McGill HC, et al, General Findings of the International Atherosclerosis Project. Laboratory Investigations, 1968, 18: (5): 498.
  5. Feinlab M, et al.  The relation of ante mortem characteristics to cardiovascular findings at necropsy.  The Framingham Study.  Atherosclerosis, 34; 145-157, 1979.
  6. Solberg LA, et al.  Stenoses in the coronary arteries. Relation to atherosclerotic lesions, coronary heart disease, and risk factors.  The Oslo Study. Laboratory Investigation,1985; 53 (6): 648-655.
  7. Okumiya N, et al.  Coronary atherosclerosis and antecedent risk factors: Pathologic and epidemiologic study in Hisayama, Japan.  American Journal of Cardiology, Jul 1, 1985; 56: 62-66.
  8. Rhoads, GG, et al.  Coronary risk factors and autopsy findings in Japanese-American men.  Laboratory Investigation, 1978; 38 (3): 304-311.
  9. Anitschkow, N.N. and Chalatov, S.  1913. Ueber experimentelle Choleserinsteatose und ihre Bedeutung fur die Entstehung einiger pathologischer Prozesse.  Zentralbl Allg Pathol24: 1-9.
  10. Steiner A, Kendall FE.  Atherosclerosis and arteriosclerosis in dogs following ingestion of cholesterol and thiouracil.  Archives of Pathology, 42: 433-444. 1946.
  11. Murata M, Kataoka S: Experimentelle Arteriosklerose und Schilddrusenfutterung. Trans Jpn Pathol8:221 –224, 1918.
  12. Turner KB: Studies on the prevention of cholesterol atherosclerosis in rabbits. The effects of whole thyroid and of potassium iodide. J Exp Med58 :115 –125,1933
  13. Libby P. The molecular mechanisms of the thrombotic complications of atherosclerosis.Journal of Internal Medicine, 2008; 263(5); 517-527.
  14. Keys, A. Coronary heart disease in seven countries.  Circulation, 1970; 41 (Suppl 1): 1-211.
  15. Roine P, Pekkarinen M, Karvonen MJ, Kihlberg J: Diet and cardiovascular disease in Finland. Lancet2:173 –175, 1958.
  16. Marmot MG, et al.  Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii, and California; prevalence of coronary and hypertensive heart disease and associated risk factors.  American Journal of Epidemiology, 1975; 102; 514-525.
  17. Marmot MG, Syme SL. Acculturation and coronary heart disease in Japanese-Americans. American Journal of Epidemiology, 1976; 104: 225-247.
  18. Longevity statistics from:  Population Division of the United Nations Secretariat, World Population Prospects: The 2000 Revision, Volume1: Comprehensive Tables, Demographic Yearbook 1999, and Population and Vital Statistics Report, Statistical papers, Series A Vol. LIV, No 1. Food intake data from: Food and Agriculture Organization of the United Nations, Statistical Database, 2000, available online at
  19. Anderson KM, et al. Cholesterol and mortality. 30 years of follow-up from the Framingham study. Journal of the American Medical Association, 1987; 257: 2176-2180.
  20. Gotto AM, et al. The cholesterol facts. A summary of the evidence relating dietary fats, serum cholesterol and coronary heart disease.  A joint statement by the American Heart Association and the National Heart, Lung and Blood Institute. Circulation, 81: 1721-1733, 1994.
  21. Yudkin J.  Diet and coronary thrombosis.  Hypothesis and fact.  Lancet, Jul 27, 1957; II: 155-162.
  22. Prior IA, et al.  Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment the Pukapuka and Tokelau island studies.  American Journal of Clinical Nutrition, 1981 Aug; 34 (8): 1552-1561.
  23. Mann GV, et al.  Physical fitness and immunity to heart-disease in Masai.  Lancet, Dec 25, 1965; 2 (7426): 1308-1310.
  24. Mann GV, et al.  Cardiovascular disease in the Masai.  Journal of Atherosclerosis Research, 1964; 4; 289-312.
  25. McGee DL, et al.  Ten-year incidence of coronary heart disease in the Honolulu Heart Program: relationship to nutrient intake. American Journal of Epidemiology, 1984; 119: 667-676.
  26. Kushi LH, et al. Diet and 20-year mortality from coronary heart disease: the Ireland-Boston Diet-Heart Study. New England Journal of Medicine, 1985; 312: 811-818.
  27. Esrey KL, et al. Relationship between dietary intake and coronary heart disease mortality: Lipid Research Clinics Prevalence Follow-Up Study. Journal of Clinical Epidemiology, Feb, 1996; 49 (2): 211-216.
  28. Tucker KL, et al. The Combination of high fruit and vegetable and low saturated fat intakes is more protective against mortality in aging men than is either alone; The Baltimore Longitudinal Study of Aging. Journal of Nutrition, Mar, 2005; 135: 556-561.
  29. Hu FB, et al. Dietary fat intake and the risk of coronary heart disease in women. New England Journal of Medicine, 1997; 337 (21): 1491-1499.
  30. Tanasescu M, et al. Dietary fat and cholesterol and the risk of cardiovascular disease among women with type 2 diabetes. American Journal of Clinical Nutrition, Jun, 2004, 79:999-1005.
  31. Paul O, et al. A longitudinal study of coronary heart disease. Circulation, Jul 1963; 28: 20-31.
  32. Gordon T. The Framingham Diet Study: diet and the regulation of serum cholesterol. In:The Framingham Study: An Epidemiological Investigation of Cardiovascular Disease, Section 24. U.S. Government Printing Office, Washington, D.C., 1970.
  33. Medalie JH, et al. Five-year myocardial infarction incidence. II. Association of single variables to age and birthplace. Journal of Chronic Diseases, Jun, 1973; 26 (6): 325-349.
  34. Morris JN, et al. Diet and heart: a postscript. British Medical Journal, 1977: 2: 1307-1314.
  35. Yano K, et al. Dietary intake and the risk of coronary heart disease in Japanese men living in Hawaii. American Journal of Clinical Nutrition, Jul, 1978; 31: 1270-1279.
  36. Garcia-Palmieri MR, et al. Relationship of dietary intake to subsequent coronary heart disease incidence: The Puerto Rico Heart Health Program. American Journal of Clinical Nutrition, Aug, 1980; 33 (8): 1818-1827.
  37. Gordon T, et al. Diet and its relation to coronary heart disease in three populations.Circulation, Mar, 1981; 63; 500-515.
  38. Shekelle RB, et al. Diet, serum cholesterol, and death from coronary heart disease: the Western Electric Study. New England Journal of Medicine, 1981; 304: 65-70.
  39. Kromhout D, de Lezenne Coulander C. Diet, prevalence and 10-year morality from coronary heart disease in 871 middle-aged men: the Zutphen Study. American Journal of Epidemiology, 1984; 119: 733-741.
  40. Lapidus L, et al. Dietary habits in relation to incidence of cardiovascular disease and death in women: a 12-year follow-up of participants in the population study of women in Gothenburg, Sweden. American Journal o Clinical Nutrition, 1986; 44 (4): 444-448.
  41. Khaw KT, Barrett-Connor E. Dietary fiber and reduced ischemic heart disease mortality rates in men and women: a 12-year prospective study. American Journal of Epidemiology, Dec, 1987; 126 (6): 1093-1102.
  42. Farchi G, et al. Diet and 20-y mortality in two rural population groups of middle-aged men in Italy. American Journal of Clinical Nutrition, Nov, 1989: 50(5): 1095-1103.
  43. Posner BM, et al. Dietary lipid predictors of coronary heart disease in men: the Framingham Study. Archives of Internal Medicine, 1991; 151: 1181-1187.
  44. Fehily AM, et al. Diet and incident ischaemic heart disease: the Caerphilly Study. British Journal of Nutrition. 1993; 69: 303-314.
  45. Goldbourt U, et al. Factors predictive of long-term coronary heart disease mortality among 10,059 male Israeli civil servants and municipal employees: a 23-year mortality follow-up in the Israeli Ischemic Heart Disease Study. Cardiology, 1993; 82: 100-121.
  46. Ascherio A, et al. Dietary fat and risk of coronary heart disease in men: cohort follow up study in the united States. British medical Journal, 1996; 313: 84-90.
  47. Pietinen P, et al. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men: the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. American Journal of Epidemiology, 1997; 145: 876-887.
  48. Laaksonen DE, et al. Prediction of cardiovascular mortality in middle-aged men by dietary and serum linoleic and polyunsaturated fatty acids. Archives of Internal Medicine, 2005; 165: 193-199.
  49. Leosdottir M, et al. Dietary fat intake and early mortality pattern—data from the Malmo Diet and Cancer Study. Journal of Internal Medicine, 2005; 258: 153-165.
  50. Morrison LM. A nutritional program for prolongation of life in coronary atherosclerosis.Journal of the American Medical Association, Dec 10, 1955; 159 (15): 1425-1428.
  51. Rose GA, et al. Corn oil in treatment of ischaemic heart disease. British Medical Journal,1965; 1: 1531-1533.
  52. Ball KP, et al. Low-fat diet in myocardial infarction: a controlled trial. Lancet, 1965; 2: 501-504.
  53. Hood B, et al. Long-term prognosis in essential hypercholesterolemia: the effect of strict diet, Acta Medica Scandanavica, Aug, 1965; 178 (2): 161-173.
  54. Christakis G, et al. Effect of the Anti-Coronary Club on coronary heart disease risk factor status. JAMA, Nov. 7, 1966: 198 (6): 597-604.
  55. Bierenbaum ML, et al. Modified fat dietary management of the young male with coronary disease. A five year report. JAMA, Dec. 25, 1967; 202 (13): 1119-1123.
  56. National Diet Heart Study, Final report. Circulation, 1968; 37: 1-428.
  57. Medical Research Council. Controlled trial of soya-bean oil in myocardial infarction.Lancet, 1968; 2: 693-699.
  58. Dayton s, et al. A controlled clinical trial of a diet high in unsaturated fat in preventing complications of atherosclerosis. Circulation, 1969; 40 (Suppl. II): 1 -63.
  59. Leren P. The Oslo Diet-Heart Study: Eleven Year Report. Circulation, Nov 1970; Vol 42: 935-942.
  60. Miettinen M, et al. Effect of cholesterol-lowering diet on mortality from coronary heart-disease and other causes. A twelve-year clinical trial in men and women. Lancet, Oct 21, 1972; 2 (7782): 835-838.
  61. Woodhill JM, et al. Low fat, low cholesterol diet in secondary prevention of coronary heart disease. Advances in Experimental Medicine and Biology, 1978; 109: 317-330.
  62. Frantz Jr ID, et al. Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota coronary survey. Arteriosclerosis, 1989; 9: 129-135.
  63. Burr ML, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet, 1989; 2: 757-761.
  64. Watts GF, et al. Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St Thomas’ atherosclerosis regression study (STARS). Lancet,1992; 339: 563-569.
  65. De Lorgeril M, et al. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet, 1994; 343: 1454-1459.
  66. Howard BV, et al. Low-Fat Dietary Pattern and Risk of Cardiovascular Disease: The Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA, Feb 8, 2006; 295: 655-666.
  67. Multiple Risk Factor Intervention Trial Research Group. 1982. Multiple risk factor intervention trial. Risk factor changes and mortality results. JAMA, 248: 1465-1477.
  68. 1984. The Lipid Research Clinics Coronary Primary Prevention Trial results. I. Reduction in incidence of coronary heart disease. JAMA 251: 351-364.
  69. 1984. The Lipid Research Clinics Coronary Primary Prevention Trial results. II. The relationship of reduction in incidence of coronary heart disease to cholesterol lowering.JAMA 251: 365-374.
  70. Hayward, RA, et al. Narrative review: lack of evidence for recommended low-density lipoprotein treatment targets: a solvable problem. Annals of Internal Medicine. 2006; 145; 520-530.
  71. Shepherd J, et al. Prevention of Coronary Heart Disease with Pravastatin in Men with Hypercholesterolemia. New England Journal of Medicine, Nov. 16, 1995; 333 (20): 1301-1308.
  72. Sacks FM, et al. The Effect of Pravastatin on Coronary Events after Myocardial Infarction in Patients with Average Cholesterol Levels. New England Journal of Medicine, Oct. 3, 1996; 335 (14): 1001-1009.
  73. Sacks FM, et al. Relationship Between Plasma LDL Concentrations During Treatment With Pravastatin and Recurrent Coronary Events in the Cholesterol and Recurrent Events Trial.Circulation, 1998; 97: 1446-1452.
  74. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. New England Journal of Medicine, 1998, Vol. 339: 1349-1357.
  75. Downs JR, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels. JAMA, 1998; 279: 1615-1622.
  76. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high risk individuals: a randomized placebo-controlled trial.  Lancet, 2002; 360: 7-22M.
  77. Shepherd J, et al. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomized controlled trial. Lancet, 2002; 360 (9346): 1623-1630.
  78. Matsuzaki M, et al. Large scale cohort study of the relationship between serum cholesterol concentration and coronary events with low-dose simvastatin therapy in Japanese patients with hypercholesterolemia. Circulation Journal, Dec, 2002; 66 (12): 1087-1095.
  79. Steinberg D, The Cholesterol Wars: The Skeptics vs. The Preponderance of the Evidence.2000; San Diego: Academic Press, Chapter 5.
  80. Libby P. The molecular mechanisms of the thrombotic complications of atherosclerosis. Journal of Internal Medicine. 2008; 263 (5): 517-27.
  81. Libby P. Inflammation and cardiovascular disease mechanisms. American Journal of Clinical Nutrition. 2006;83(suppl):456S-60S.
  82. Tontonoz P, Nagy L, Alvarez JG, Thomazy VA, Evans RM. PPARgamma promotes monocyte/macrophage differentiation and uptake of oxidized LDL. Cell.1998;93(2):241-52.
  83. Laufs U, Fata VL, Plutzky J, Liao JK. Up regulation of Endotelial Nitric Oxide Synthase by HMG CoA Reductase Inhibitors. Circulation. 1998;97:1129-1135.
  84. Nenseter MS, Drevon CA. Dietary polyunsaturates and peroxidation of low density lipoprotein. Curr Opin Lipidol. 1996;7(1):8-13.
  85. Nagy L, Tontonoz P, Alvarez JG, Chen H, Evans RM. Oxidized LDL regulates macrophage gene expression through ligand activation of PPARgamma. Cell. 1998;93(2):229-40.
  86. Mozaffarian D. et al. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women.  American Journal Clinical Nutrition.2004;80:1175-84.
  87. Herron KL et al.  High intake of cholesterol results in less atherogenic low density lipoprotein particles in men and women independent of response classification. Metabolism.  2004 Jun; 53(6); 823-30.
  88. Fernandez ML.  Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations.  Curr Opin Clin Nutr Metab Care.  2006; 9:8-12.
  89. Warensjo E et al.  Estimated intake of milk fat is negatively associated with cardiovascular risk factors and does not increase the risk of a first acute MI.  A prospective case-controlled study.  British Journal of Nutrition.  2004 Apr; 91(4); 635-42.
  90. Biong AS et al.  Intake of milk fat, reflected in adipose tissue fatty acids and risk of myocardial infarction: A case control study. Eur J Clin Nutr.  2006 Feb; 60(2); 236-44.
  91. Rausch HP, et al. The influence of calorie restriction and of dietary fat on the tumor formation with ultraviolet light. Cancer Res, 1945; 5: 431.
  92. Carroll KK, et al. Dietary fat and mammary cancer. Can Med Assn J, 1968; 98: 590.
  93. Pierce ML, Dayton S. Incidence of cancer in men on a diet high in polyunsaturated fat.Lancet, 1971; i: 464.
  94. Bursten SL et al.  An increase in serum C18 unsaturated free fatty acids as a predictor of the development of acute respiratory distress syndrome.  Crit Care Med.  1996 Jul; 24(7); 1129-36.
  95. Aviram M et al.  Pomegranate juice consumption reduces oxidative stress, atherogenic modifications to LDL, and platelet aggregation; studies in humans and in atherosclerotic apolipoprotein E-deficient mice.  Am J Clin Nutr.  2000 May; 71(5); 1062-76.
  96. de Rijke YB, Bredie SJH, Demacker PNM, Vogelaar JM, Hak-Lemmers HLM, Stalenhoef AFH. The Redox Status of Coenzyme Q10 in Total LDL as an Indicator of In Vivo Oxidative Modification. ArteriosclerosisThrombosis, and Vascular Biology.1997;17:127-133.
  97. Dou X et al. Curcurmin up-regulates LDL receptor expression via the sterol regulatory element pathway in HepG2 cells. Planta Med, 2008 Sep, 74 (11): 1374-1379.


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Imagine What Could Be Possible If People Quit Believing The Lies!!!

Hello Journey Fans.

As I sit here watching a baseball game on TV conversing with my friends in the IPMG Group on Facebook, I am reflecting back on a response to a post on a very popular weight loss TV show page.  I have had several friends share my post, and I realized that I must share it with all of you too as I hope that you can share it with your friends, family, and co-workers in an effort to get the word out about getting out of the “DIET” mentality, and embark on a “LIFESTYLE” change to just eating REAL FOOD!! That’s really all this is about.

I will not link that TV show page on my blog, as I find it just very sad now to what they do to these people, as they are just trying to find the fattest humans on the planet to put them through ridiculous amounts of working out and eating such crappy commercialized processed packaged nasty food, low fat, high carb, cooking GMO veggies using GMO hydrogenated oils and calling it all “heart healthy”!! It makes my stomach turn.  If you happen to be on Facebook and go to that page, it’s not hard to find the post near the top of the page about “Canola Oil”  There were several people in that post arguing how great it was, and several of us IPMG members posted many links showing what a poison it was, and that it was originally used for a biodiesel fuel.  One woman in particular made several comments, kept saying that it was fine as long as it was “COLD PRESSED” (which is garbage) and we all countered her points, and finally she just got tired of it, and she deleted every single one of her comments, at least 10 in all.  So the thread reads a little weird, but you can see that it’s amazing that when some people clearly are outclassed and out info’d they tuck tail and run.

All we wish to do is help folks do some research.  To not believe all the lies we’ve been fed, and to realize that everything the government has created with regards to our food system is just PLAIN WRONG! It doesn’t work, it has made us the fattest country in the world, it has made us more sick and diseased than at any time in the history of our existence, and that they should stay out of our homes, our farms, our lives, and just let people GROW FOOD and RAISE ANIMALS the way that NATURE does!!

(BACKGROUND) Someone in the thread posted a link to their website (for a diet plan/supplement site/expensive garbage) and said do this and you’ll have “no regrets.”

My response from there…
(name) we have no regrets…except perhaps we didn’t start or know about this lifestyle 5, 10, 15 years ago!!! This isn’t a diet in the sense of the context of what this page, and what you all know and have yoyo’d with your entire life just like I did, and others have. 

This is a lifestyle!! A way of eating real food that you will do for the rest of your life…Never starving yourself, never depriving yourself of good food, and it will be the only way you WANT to eat for the rest of your life!! If you truly want change and stop the “dieting” roller coaster then you will change your life forever!! 

I watch the BL for years, and what the folks have done on the show has been nothing short of incredible, but this way is NOT SUSTAINABLE! Just look at past winners who have gained all the weight back because of their ADDICTIONS to crap food that you all think is “healthy”. 

We put the emphasis on QUALITY REAL WHOLE FOOD. We take pride in finding a local farm source for meats, and vegetables, and fruits, eggs, and pride ourselves in “not living out of a box” or a “fast food” restaurant. Because it’s the corporations, and the subsidized grain industries that make all your “diet products” filled with chemicals, and soy, and canola/vegetable/seed/hydrogenated/disgusting waste products that you ingest everyday because it says “heart healthy fat” on the label. 

Real food has no label!! We take the time to research and know what we put in our bodies. If everyone would stop using “convenience” as an excuse to eat crap, imagine how much we could put into our system to change the thinking instead of becoming more sick and diseased as this nation has become. 

There are cures for cancer, diabetes, rheumatoid arthritis, multiple sclerosis, and hundreds of other so called “incurable” or you’ll have this the rest of your life ailments that you can ELIMINATE WITH FOOD!! Until I embarked on this lifestyle over a year ago, I was just like you all…looking for the quick fix, looking for the answer, looking for the way. Well I’m here to tell you, I found the way and I have no product, pill, shake, or secret that I will make you pay for. I, and many others will freely help you and guide you at no cost for info, and if you take the time to invest in yourself, you will see that what I say is TRUTH. You have to trust yourself, and we have a support network of folks, and a movement of people who are sick and tired of being sick and tired. You trusting a system that doesn’t care one bit about your being healthy is what is killing millions, and prolonging life with pills, procedures, and a cycle of lies that you all buy into every single day. 

Here are some free sites with tons of info and links that you can use every day for guidance and help should you decide to invest in your “true health” Meats, eggs, saturated fats from pasture raised animals, coconut products, extra virgin olive oil, avocados, veggies, fruits, nuts. These foods are all you NEED to thrive and live a very healthy and happy life. Obviously if you have allergic to things like eggs or nuts, just don’t eat those. It’s all about quality!! Know where your food comes from!

You want a success story, here ya go. I know this man, speak to him almost daily, and he is REAL. He is one of the finest humans on this planet, and I am proud to call him friend even though we have never met in person.

Animals, Plants, Water…it’s not hard folks. Being diabetic is hard, being sick is hard, having cancer is hard. Imagine a life free of those things because you PREVENTED it just by eating real food. 

The only person who can be the Expert of you, IS YOU!! All the advice that anyone gives you must be questioned and tried out on you, by you, in order to make an informed decision to decide if that was RIGHT or WRONG for YOU!! No special schooling is necessary, you don’t need a college degree or a medical degree, or a nutritional degree to eat real food and see if it works or not. Self experimentation is the only way to truly know what works FOR YOU!!

If someone tells me they CAN’T ever give up Bread or Pasta or their beloved Oatmeal, cookies, cakes and sweet stuff, and they never give a reason other than “Oh I could never do that, or eating red meat will give you cancer, or all that fat will make me fatter, or you’ll get high cholesterol eating all those eggs.” That is where the world has been fed a great big lie!! All those who still believe it (because they haven’t been convinced otherwise by trying something new) They are the ones that truly need the most help. They are in such a brainwashed state of denial that they are UNWILLING TO EVEN TRY to get past the thinking, past that “you are afraid of me being right” stage. 

I can’t means…I Certainly Am Not Trying Those words ring in my head every time I hear someone say I can’t do something.

Get past the DOGMA people. If you never attempt to live this way, you will never know if it’s right or wrong FOR YOU. Don’t just say it doesn’t work, or you could never do that, because that just means you are afraid of being wrong.

Good luck to you all. If you want something you’ve never had before, you have to do something you’ve never done before!! Take a look DEEP WITHIN yourself, and find that motivation to finally break free and never live a life of “dieting” again. I did, and it saved my life!! YOU CAN TOO!!! Take your health back into your own hands. There are plenty out there who will give you the support you need free of charge, and I’ve given you plenty of resources to get started on REAL LIFE today.

So there ya go.  The thread continued on with even more people posting how they think we’re all crazy, that because we “aren’t dietitians” we don’t know what we are talking about, and that is what is most sad.  I have more knowledge based on my own research than they will ever teach in a book, or course, can supply hundreds of medical posts, links, and studies, yet people still believe what the system of lies tells them.  The ones that have broken through and are like me and finally figured it out continue to attempt to educate, and many will never get it, but we will keep trying, we will keep posting, we will keep supplying the latest and greatest info we can find to help people finally reach that point where they WANT CHANGE, where they are tired of being sick, and diseased, and broken.  If what I posted can help just one person of the 1.5 million plus fans of that page, then it’s all worth it!! Because that person will then tell their friends, family and co-workers and the cycle shall continue!!

Take back your health!! It’s truly all we have that’s ours and what we can control!!

Every man dies.  Not every man really lives. – Braveheart

How many of you wish to “really live?”  I sure do, and I am!!!!

Make the choice to do the same!!! YOU WON’T REGRET IT!! 😉


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Big Tim’s Chipotle Hickory BBQ Sauce

Hey Journey Fans!!

As tomorrow is the 4th of July, and I’m sure many of you will be spending time with family and friends outdoors grilling some awesome meats and veggies, and I thought it was time to post my own BBQ Sauce!! I’ve played around with a few different ones from some of my friends over the past few months, and the time has come for me to create and post my own.  This came out Awesome!! It has a nice Hickory flavor, and a great bite with the Chipotle Pepper.  I will be using this quite often for Ribs, Pulled Pork, Burgers and BBQ Beef.

Big Tim’s Chipotle Hickory BBQ Sauce

3 cups Organic (or homemade) Beef stock.
2 cans 6oz each Organic Tomato Paste
1 Sweet Brown Onion
2 Tbsp Minced Garlic or 3-4 cloves chopped fine
2 Tbsp Dijon Mustard
4 Tbsp Raw Apple Cider Vinegar
3 Tbsp Extra Virgin Olive Oil
4 Tbsp Chili Powder
2 Tbsp Raw Honey
2 Tsp Sea Salt
2 Tsp  Black Pepper
2 Tsp Chipotle Pepper
2-3 Tbsp Liquid Smoke

Take your Onion and Garlic, and throw it in your food processor/blender/Ninja/Vitamix whatever you have, and process it super fine.  When you reach your desired consistency add to stock pot.  Turn on heat and brown onion and garlic for 3-5 minutes to release the flavors.

Add all remaining ingredients to the stock pot, and stir till all incorporated.  Bring to a boil.  Reduce heat to very low, and simmer for 1 hour, stirring occasionally.

After one hour, taste, and adjust accordingly.  If you want it thinner, add some more beef stock and simmer 15 min longer, may need extra salt, or liquid smoke, or more pepper.  Let cool, and jar it up for later use.  Store in refrigerator.

Have a safe and fun Holiday!






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