Low saturated fat low cholesterol eating plan,how to look younger at 40 uk list,lose weight fast no diet no exercise equipment,best way lose weight while breastfeeding 911 - New On 2016

15.10.2014
A few weeks ago a friend asked me If I had an opinion on a story he’d seen about low cholesterol being linked to high suicide rates. So you can see that back in 2000 I wasn’t doing too badly and everything was in the right range, except resting heart rate which was on the high side and bizarrely LDL cholesterol was a little low!
What is perhaps most interesting, is that last year I really went off the rails and put a load of weight on. Did you see the BBC had a story yetserday about the proposal to offer Statins etc to those at 55 or over because it’s more cost effective? Hi Lawraine, both being 7 does appear to be high, but cholesterol is only a correlated symptom of heart disease, not a risk factor (in my opinion). How do you think the results would be affected if you ate the same diet but were not fit and active? I saw a program that showed how external appearance is no indicator of health as measured by fat deposits i.e a slim person with a poor diet (lots of convenience foods etc) can still have fatty deposits in an around internal organs. Forgive my ignorance but would you know if cholesterol levels are any way an indicator of how much fat is stored in the body? I don’t think that cholesterol levels are directly an indicator of how much fat is stored in the body, though I would guess that the 2 generally go hand in hand.
Great post Colin, its amazing how people seem to instinctively think that meat must be bad for you. Apart from the contrary dietary advice , his argument that higher cholesterol levels can be linked to longevity in other cultures ,and that lower levels are actually dangerous to the extent that they can increase the risks of cancer are persuasive , to say the least .
Indeed you’re right James, but then it seems the world can only manage to economically feed 7Bn people by feeding them a poor diet. They did say at the time my LDL was below normal back then, but the advice seems to have changed recently. I eat 3-4 whole eggs every morning, 5 days a week, plus I love high cholesterol food and my levels are in the normal range. Those wishing to reduce their cholesterol through a change in diet should aim to consume less than 7% of their daily energy needs {metric units Joules (J) or (kJ), pre-SI calories (Cal) or (kcal)} from animal fat and fewer than 200 mg of cholesterol per day.
Although a diet high in saturated fat is the main cause of high blood cholesterol levels, high cholesterol in the diet can also raise blood cholesterol levels. When the Framingham study found a correlation between heart disease and cholesterol levels, the assumption became that eating eggs was bad, since eggs include high level of cholesterol. Over the last 18 months, I virtually eliminated (bad) saturated fat from my diet and my levels are now near normal (as others have said, dietary cholesterol is now thought irrelevant).
If you read that Great Cholesterol Con book I mentioned, Dr Kendrick reveals that statins are *never* beneficial for women to take, not when you look at total mortality figures, so it looks like you made a good choice there. I appreciate the corrections and am rather embarrassed that I didn’t spot those typos myself. The cholesterol hypothesis links cholesterol intake and blood levels to cardiovascular disease. Apparently, the hypothesis is false and should be buried.The historical background to the hypothesis of a causal relationship between the level of serum cholesterol and the development of atherosclerosis beganwith Rudolf Virchow ’ s description (1856) of the atherosclerotic plaque with its cholesterol deposits. Two publications by Ancel Keys had a tremendous impact on the general belief of the cholesterol hypothesis. These studies showed clearly that there is no causal relationship between the cholesterol level in blood and the risk of dying from a myocardial infarction but the so-called cholesterol hypothesis is still alive. To answer that question, one must consider the pivotal role powerful drug companies have increasingly played in relevant research and publications.
As pointed out in the newly published books, White Coat, Black Hat (Carl Elliot) and Medical Research for Hire (Jill Fisher) many of these trials are accomplished by Contract Research Organizations (CROs). In an excellent and unmasking article Michel de Lorgeril and Patricia Salen (7) reviewed and discussed the cholesterol-lowering drug trials published before and after the Vioxx affair was disclosed in 2005 (which resulted in new clinical research regulations).
A population based investigation in Sweden (9) including almost 2 million men and 2 million women found that despite a widespread and increasing utilization of statins during the years 1998 to 2002 there was no correlation to the incidence or mortality of acute myocardial infarction. In summary, we have now an overwhelming amount of scientific data that falsify the cholesterol myth. Thanks for your comment Murat, I’ve editted it to improve the formatting, readability and highlighted some key points. Atkins diet and low carb discussion provided free for information only, not as medical advice.
Background: In October 2011, the British Journal of Nutrition published a guest editorial by 13 scientists (Pedersen et al). The articles contain a lot of information, so I decided to go for a stepwise analysis of the contents. Uncertainty has recently been expressed as to the role of SFA for the development of atherosclerosis and CHD. Our main concern, however, is to emphasise the importance of lowering SFA intakes to reduce blood LDL-cholesterol levels at a time when there are tendencies to downplay the importance of SFA.
I was surprised about the 2nd sentence, because the importance of HDL-cholesterol in this association was not mentioned. Results suggest that isoenergetic replacement of SFA with carbohydrates does not improve the serum total:HDLcholesterol. Results of prospective observational studies, controlled clinical trials with drugs, mechanistic studies, and genetic 'experiments of nature' all strongly suggest that high concentrations of HDL-cholesterol in the circulation help to prevent coronary artery disease and other CVD.
The effects of dietary fats on total:HDL-cholesterol may differ markedly from their effects on LDL. And in 2007, a meta-analysis of 61 prospective studies article was published in the Lancet (6). In 2011, the authors completely changed their mind, while they did not reject de results they published earlier. There have been substantial reductions in mortality from CVD (cardiovascular diseases) in North America, Western Europe and Australasia over the last 30 years that reflect successful national public health policies to reduce the intake of SFA (saturated fatty acids), in addition to promoting smoking cessation and controlling blood pressure. A report from the US Department of Agriculture and the US Department of Health and Human Services states that no reductions were found in the intake of SFA in the American diet over the period 1989?1 to 2005?6. More importantly, it is not possible to unequivocally associate changes in SFA intake to changes in CHD mortality over time, since many changes in diet, lifestyle, diagnosis and pharmacological treatments have occurred over the last 30 years.


That replacement of SFA by a variety of carbohydrate-containing foods also reduces CHD risk may be inferred from ecological studies, e.g. Hoenselaar expresses doubt if a reduction in SFA intake has occurred concurrent with the decline in CHD mortality in developed populations. During several decades before the turn of the 20th century, SFA intake declined and PUFA intake increased in the USA. I also showed that both heart disease and stroke mortality are highest in countries with low saturated fat consumption. Conclusion Part 2: An international group of scientists states that mortality from cardiovascular diseases has decreased over the past decades. Background: In 1993, Artaud-Wild et al published an article linking per capita intakes of saturated fat to mortality rates from coronary heart disease (CHD) (15).
Results: unexpectedly, the highest mortality rates from CHD were found in the countries with the lowest intakes of saturated fats. Conclusion Part 3: a global analysis including 40 countries showed that higher intakes of saturated fat were linked to higher mortality rates from coronary heart disease among men in 1977. 6) Prospective Studies Collaboration (2007) Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths. 7) US Department of Agriculture and US Department of Health and Human Services (2010) Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010.
10) Committee on Diet and Health (1989) Dietary intake and nutritional status: trends and assessment. I found the whole thing very interesting and saddening (the obtuse scientists always sadden and frighten me). As it happens I DID have an opinion on this, none of it complimentary about low cholesterol diets or Statins, the cholesterol lowering drugs. We’re talking steak, fatty mince meat (ground beef), pork of all forms including roasts with crackling, and bacon, oh yes plenty of bacon!
So much so, that my daughter now eats just like I do and when my friend asked me about low cholesterol issues, I resolved to get myself tested to prove that I was right, so I did and the results are back. I was starting to put weight on though on my fairly typical western diet of cereal for breakfast, sandwiches and crisps for lunch, and typically meat and 2 veg type dinner (or pasta, pizza, curry, Chinese etc), with an occasional desert. CrossFit got me exercising and onto the Zone Diet and then with heavy Paleo Diet influences + dairy. I never bothered much about cholesterol, but recently I thought I ought to get checked out. Unless you happen to have had a heart attack already, and are a middle aged, obese man, statins won’t help.
I assume that this impact on health would show by increased blood pressure, resting heart rate and respiritory values. Dietary cholesterol does not increase your LDL cholesterol level, I don’t know where you have heard that claim. Our family has been identified as having hypercholesterolemia – pretty common in people in the North of England and Scotland, and genuinely scientifically proven in that they can observe the difference in how the body processes certain types of fat. It has actually been a long time since GPs in the UK thought that the diet-heart-disease link applied to every individual. I suspect you already realise that $$$ is at the heart (pun intended!) of the statin pushing drug companies in the US. I enjoyed reading all of this information, and applaud you for your intense research, and dedication to such a topic! It has had enormous impact on health care and society during decades, but has little or no scientific backing that is relevant for the human species. Nikolai Anitchkov’ s experiment with rabbits in St Petersburg (1913) was a key publication. In 1953 he reported that the dietary intake of fat was significantly correlated to the serum cholesterol level and the incidence of cardiovascular death in six countries (1). It was found that the cholesterol level had been slightly increased after a heart attack in previously healthy men.
Sachdeva and coworkers (5) found that the cholesterol level in patients with acute myocardial infarction was substantially lower than in normal controls at the same age. The most momentous arguments for keeping the idea alive are the reported beneficial effects of cholesterol-lowering drugs – the statins. Before the Vioxx scandal the dominating part of the published statin trials were highly positive, especially in the secondary prevention trials. This is in harmony with the meta-analysis of Ray et al (10) showing no prolongation of life by use of statins in randomized controlled trials involving 65 229 participants.
Bernstein Diabetes Solution and any other healthy low-carb diet or plan, all are welcome in our lowcarb community. In this article, they explain the importance of reducing saturated fat intake to limit heart disease risk (1). Two (Katan MB and Mensink RP) of the 13 scientists involved have published an article in the past (5). All natural fats contain both SFA, which do not change this ratio, and unsaturated fatty acids, which lower it. Given these observations, it appears imprudent to ignore the marked effects of diet on HDL-cholesterol. The effects of fats on these risk markers should not in themselves be considered to reflect changes in risk but should be confirmed by prospective observational studies or clinical trials. They stressed that the effect from dietary fats on HDL-cholesterol should not be ignored and that effects on cholesterol should not in themselves be considered to reflect changes in heart disease risk.
All of a sudden, changes in LDL-cholesterol - and LDL-cholesterol only - are supposed to be the single one predictor of changes in heart disease risk. If these changes occur at the same time, how do we know which change "caused" any possible change in CVD? There are also reports of declining SFA intake concomitant with the reduction in CHD mortality in several other populations. No correlations were made between saturated fat intake and heart disease in any of the articles referred to.


If there is a large absolute increase in carbohydrate intakes over the past decades in the USA, the relative contribution of saturated fats will automatically decrease. Heart disease and stroke mortality are highest in countries with low saturated fat consumption. But in 2008, the British Heart Foundation published the European Cardiovascular Disease Statistics (16).
Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Explaining the 25-year decline of serum cholesterol by dietary changes and use of lipid-lowering medication in Finland.
Differences in coronary mortality can be explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and Finland.
Add to that cholesterol laden eggs, hard cheese, full fat soft cream cheese, sausages, fatty lamb (both leg and shoulder) and whole (full fat) milk, not to mention glorious double cream!
This year I’ve sorted myself out and in 3 months have lost the weight I put on last year.
My HDL and LDL were both 7 something, which are very high, but the doc said that they cancelled each other out and I needn’t worry.
I think I’ll start carrying my test results in my wallet, show them to anyone who says that. He fed rabbits with cholesterol from egg yolks and found that they developed atherosclerotic plaques containing cholesterol. It appeared very convincing but the problem was that these six countries were selected from all together 22 countries.
Therefore, it was claimed that high cholesterol was a risk factor for myocardial infarction. Al-Mallah and coworkers (6) found lower LDL values in patients with acute myocardial infarction and also that the mortality rate was twice as high among patients with the lowest LDL values. Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With the Guidelines. Low admission LDL-Cholesterol is associated with increased 2-years allcause mortality in Patients with non ST segment elevation myocardial infarction. Statins for the primary prevention of cardiovascular disase (Review) The Cochrana Collaboration. Statin and all cause mortality in high risk primary prevention: a meta-analysis of 11 randomised controlled trials involving 65,229 participants. As a result, even the replacement of dairy fat and tropical fats with carbohydrates will increase the ratio of total to HDL-cholesterol.
The reason why the relative contribution showed a small decline, is that intakes of energy from other nutrients (in this case carbohydrates) increased even more.
What these articles actually described were trends in fat intake over different time periods for three different populations.
Since these three changes were of equal size and took place at the same time, it will take other data to put them in perspective before they can be possibly directly linked to CHD. The report included European mortality rates from both CHD and stroke for 1972 to 2005 for both men and women. But I realised I hadn’t got my blood worked up since starting my new way of eating and so I did.
What if I’d been wrong all this time and was eating myself to death, however enjoyable it was doing so?
When he tried with other animals –carnivores– it was not possible to reproduce the results. Amazingly, very little attention was taken when the 30 years follow-up of the Framingham project was published(4). A Cochrane study including 14 primary prevention trials with statins was recently published (8). This was followed by a response by Pedersen et al (3) and again, by a response from me (4). Therefore, the strongest change is an absolute and relative increase in carbohydrate intake. The decline has been particularly noticeable in the Finnish population that has experienced the most rapid fall in CHD mortality in the world. I find it very disturbing that a group of 13 scientists draws firm conclusions, but is not able to find one single study as a base for their findings. In addition, it provided data about European per capita consumption of saturated fat for the year 1998. It turned out that high cholesterol was not a risk factor for men older than 47 years and not for women at all. The most obvious conclusion would then be that an increased intake of carbohydrates (or small increase in saturated fat intake) was linked to lower mortality from CVD.
This data gives us the possibility to link saturated fat intake to mortality rates in 1998.
Further, it was found that more men had died of a heart attack among those whose cholesterol had decreased over the years. A total of 41 countries had available data about both saturated fat intake and mortality rates for this year.
Keys followed 12000 middle-aged men and recorded their diet and cholesterol values for many years.
The New Zealand report is the only article which might suggest a direct link between SFA and CHD. I used a simple Pearson correlation to examine if a significant correlation could be found.
It shows a trend in decreased CHD rates over time, and (in another part of the text) it is mentioned that SFA consumption decreased over time.



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