Once upon a time, the rhetoric around statins was relentlessly positive. More recently, though, I think there’s been increasing numbers of doctors and commentators expressing concern about the limited effectiveness of statins, as well as their known but perhaps under-recognised risks. A few weeks back an Australian documentary aired that featured several quite-conventional doctors and academics who expressed considerable scepticism about statins. You can see the documentary on YouTube here.
I’ve noticed reports this week from doctors who have expressed concern that since the airing of this documentary, many patients have taken matters into their own hands and stopped their medication. The general tone of these reports is been that the documentary has encouraged individuals to put their lives in perilous danger. But let’s leave the rhetoric aside for the moment. What are the real risks of stopping statin medication? Does stopping a statin really increase the risk that someone will ‘have a heart attack and die’?
The great majority of people taking statins have no history of heart attack or stroke, and the idea of taking statins is to prevent such an occurrence – so-called ‘primary prevention’. In this context, statins do not save lives. For healthy individuals, then, the evidence shows that countless individuals might stop their statins, but not one of them will lose their life as a result.
What might happen to the risk of having a non-fatal heart attack, though? Well, the data here shows that in primary prevention, 300 people will need to be treated with statins for a year to prevent one heart attack [1]. So, if someone were to come off their statins for a year, the risk of them having a heart attack as a result are actually tiny (about one third of one per cent). Even if we multiply this figure over several years, the risk still remains very low.
In individuals with a prior history of heart attack or stroke (‘secondary prevention’) the benefits of statins a greater. In this context, for example, statins do reduce the relative risk of death (particularly from heart attack). However, again, this benefit needs to be taken in the context of underlying risk. The data show that if 200 people were to be treated with statins for a year about one person would be spared a heart attack. If 100 people were treated, only about one life would be saved over the next five years [2]. Taking all benefits into consideration, over five years of treatment, 96 per cent of people would not benefit at all.
This means, again, that if even if someone has had a prior heart attack, stopping statins is actually quite unlikely to usher in a heart attack or earlier demise.
It’s only by taking a cold hard look at the data and understanding it in real terms that we can make an accurate judgment about the supposed risks of stopping statins. I think we doctors do a huge disservice to people by either not being aware of the data or giving patients a false impression of the risks of stopping statin therapy.
References:
1. http://www.thennt.com/nnt/statins-for-heart-disease-prevention-without-prior-heart-disease
2. http://www.thennt.com/nnt/statins-for-heart-disease-prevention-with-known-heart-disease/
I’m curious how many people on statins for primary and secondary prevention will STILL have heart attacks?? Are there studies?
Drug companies seem to imply that taking statins will absolutely prevent heart attack, but I suspect that cannot be true.
I have already documented my history on your excellent site, but at risk of repetition, maybe I can throw some evidence in support of your article.
March 2013…
taking Simvastatin 40mg, Metformin 2g, sitagliptin 100mg, pioglitazone 30mg, candesartan 8mg.
Overweight, Indigestion, abdominal bloating, lethargy, etc etc..i.e. sad and prematurely old.
GP having a dicky-fit at my suggestion that I reduce any meds, but offering no alternative, except a dire warning of impending doom if I dare to do so.
December 2013…..
Taken matters into my own hands. Researching, then implementing a complete lifestyle change…
Alive and kicking. No medications at all. Slim, comfortable gut and energised. Happy!
I do not advocate any person to follow my example….I merely tell my tale.
That was a nicely done show in Australia on statin drugs and heart disease treatment overall. I recall reading similar on Dr. Eade’s sight sadly about some physicians claiming people will die due to the show, leading people to stopping their statins. It had me thinking, how remarkable.
What if we changed the name from statins being ineffective at helping most with preventing cardiacs with any of the three – fish oil, aspirin or niacin. Studies have been done on fish oils, aspirin and niacin helping prevent heart attacks. Many doctors for years have recommend the three to patients. Yet, over the last few years a few articles have come out saying all three might not be as helpful at preventing cardiacs as we have long thought. When that happened I don’t recall hearing an out cry of concern from a few physicians saying that now people will die from what the articles say because people will stop taking their fish oil, aspirin and niacin.
I’m not surprised by the response, sadly. Hopfully those that do stop taking statins and are wanting to take charge of their health will look into other possible helpful ideas such as low sugar diets, heart CT scans for detection, thyroid testing, nutritional status and other heart disease prevention ways.
The poor relative benefits of statins are the unrealistic BEST-CASE scenario. As Dr Ben Goldacre has shown, pharmaceutical companies often only publicise the most favourable studies, leaving mediocre or bad news shut away in a drawer. And the studies that they do publicise are very careful to stack the deck in their favour (careful exclusion policies, odd termination criteria and so on). Every year, the companies are caught doing this, and then pretend to have learned their lesson. Until the next revelation pops up, like clockwork.
Thus, it is not some mad conspiracy, but Occam’s-razor-rational to assume that a true and honest meta-analysis of ALL the trials related to statins (including the ones conveniently languishing in dark drawers) will reveal that even those paltry benefits you outline are overstated.
Now that ever-more statins are coming off patent, though, non-generic drug companies will suddenly want to dismiss them in place of the new lucrative mega-drugs like PCSK9. “What? Statins? Those old things? Hah!”
Here’s my prediction, therefore: I think we’ll find that, as with so many other drugs that enter the public domain (SSRIs etc), their effectiveness for even their original treatment group will become increasingly indistinguishable from placebo.
Jennifer – “While statin drugs have demonstrated a very modest ability to prevent a second or third cardiovascular event in male patients diagnosed with heart disease, they have shown no positive benefit in primary prevention (a first event). This is not due to their cholesterol-lowering effect, but rather their mild anti-inflammatory benefits. However, this can be achieved by any number of natural inflammation-fighting substances, including fish oil and curcumin (turmeric). Statins provide little to no protection for otherwise healthy individuals who exhibit elevated cholesterol.
Moreover, studies have shown that elevated cholesterol is actually protective against all cause mortality (including cardiovascular events, in menopausal women. The greatest benefit that statin drugs provide is to make their manufacturers wealthy how these companies managed to convince the medical community and the general public that millions of us needed to be on these drugs remains one of the greatest unsolved medical mysteries of our time.” – (Excerpted from my new book, The 30-Day Blood Pressure Cure, co-authored with Roy Heilbron M.D., who was the co-creator of the South Beach diet along with Arthur Agatston, M.D.)
The sham of cholesterol-lowering was recently exposed by a recent study showing that of almost 140,000 patients admitted to the hospital for heart disease, almost half of them had LDL levels under 100 mg/dL (the therapeutic target for LDL for the past few years). This is from the excellent book, The Great Cholesterol Myth authored by renowned cardiologist Stephen Sinatra, M.D.
And as far back as the famous Framingham research, we have known that cardiac events occur equally in patients with total cholesterol below 150 as in those with levels 300 and higher.
Very new research shows metformin, which you admit you are on, has protective cardiovascular effects for women. But if you would like to be able to discontinue it (while losing weight along with your Type 2) may I suggest you take a look at The 30-Day Diabetes Cure? Respectfully yours, Jim Healthy
We are just going to launch into another concentrated study, in order find a cure for Alzheimer’s. I couldn’t fail to notice that Mr Cameron mentioned ‘massive investment from the pharmaceutical industry to fund research’. What’s the betting the drug they find, (if any) will be yet another ‘management drug’, rather than a cure. I don’t think these people want to cure any off these diseases. Why, for instance, should they try to they find a cure for diabetes, when they make millions from selling insulin to the NHS, just to manage the condition? Alzheimer’s offers them the same opportunity. Find a drug to manage the condition, and halt the disease’s progress. Magically, there’s another ready cash-cow for them. Find a drug to cure the disease? Not likely. That wouldn’t be in the interest of the shareholders. Call me a cynic, but I think I am right.
The main reason statins are recommended by pharmaceutical companies is that it creates more revenue for them. Unfortunately, once a doctor has graduated, it is usually the pharmaceutical representatives that “educate” them about what their patients require to maintain health or “prevent” issues such as heart attacks from occurring. Follow the money and it will show where interests lie. Like most things in life, it is only ourselves who have a vested interest in keeping us healthy and it is not the lack of a particular drug that causes ill health but usually lack of an essential nutrient and/or exercise, that leads to diseases and disorders.
Statin drugs come with instructions to use them in combination with a low-fat/low-cholesterol diet and I doubt that they have ever been studied in people who refused to follow the directions for taking them. Any tiny advantage they seem to have for preventing heart attacks in some people would likely disappear without the low-fat diet requirement. Just changing the diet to include more natural fat and fewer carbs would out-perform the statins, but the drug companies are unlikely to ever fund such studies.
Thank you Jim Healthy.
When I said to my GP that I intended to ‘go it alone’ to get off all my medication, (because there was going to be no help from the surgery to accomplish my wishes),I was told that under no circumstances should I ever stop the metformin, even if I weaned myself off all the others.
But I researched metformin too, and did not like what I read. So…..I no longer take medication of any sort.
I use a low carb, high fat diet. I have now lost 30lbs in weight.
After the festive season , which is in no way going to be over indulgent in our household, I intend to tighten up my diet even further, and aim for a more ketogenic state. My blood profile and B/P show no reason to go anywhere near my GP.
However, I will consider what you have said about the protective findings of metformin for women.
My concerns about all the meds I was taking was with regard to the risk of each one, alongside the cumulative multiplier effect of all 5, which at age 65 I thought ought to be
considered.
Jennifer.
How strange that after I began my accursed statin treatment, I began to positively lust after fatty food, which I’d been quite restrained about previously. Maybe my body was trying to tell me something………
In 2004, my father, then 73, discovered that what he thought was flu had been a heart attack. One artery with a 90% blockage. With some recovery time and a stent, he was sent home and placed on the usual blood thinner/statin regimen. The past two years he saw a gradual weakening of his legs, to a point at which, after several falls, he was hospitalized and found in September to have a brain tumor. His surgery was deemed successful, but it appeared that he was slipping towards dementia. He never rallied, and died in November. My dad’s diet had been horrid for years, the usual processed grains and sugar forming more than half, but I do wonder now if statins may have played a role. He was dealing with elevated sugars the last year, with all the feet and ankle swelling, mood swings, etc. and the surgeon was clear that the type of cancer was one he could not have had longer than 6 months. Perhaps just speculation…..
Testimony.
After having started my LCHF diet (LowCarbHighFat), lost 15 kg I decided to throw away my 40 mg LIPITOR statins and after this I started to feel strong and healthy (up till this day).
Best
LCHF@MatsWiman.se
Good start Dr Briffa!
I think there is another side to the coin: dangers of taking statins- see 2.
1/ Lets not forget that it is the small dense LDL particles that are dangerous. The large fluffy are not. There are no statins reducing only the bad LDL statins reduce both bad and good large particle LDL. Same for Becel and Benecol and all margarin spreads BTW. Statins also reduce the good HDL. But by reducing sugar and fast carbs (bread, pastas) the dangerous small LDL particles ONLY reduce and HDL rises and triglycerides drop at same time. If you want to know real risk factors measure ApoB/ApoA. If your doctor don’t know or dont want to find out, please change doctor before it is too late!
Going low carb like LCHF will remove all small LDL and improve the rest of the markers of metabolic syndrome like high VLDL,
hypertension and inflammations. And stabilize blood sugars of course.
2/ Dangers of low cholesterol. Studies – done by pharma companies – have shown that
there is a risk increase for hemorrhagic stroke when taking statins, but only if one has had a stroke already.
The problem for us is that there are no other study results published of hemorrhagic stroke or other blood vessel break down and statins. Since the research presumably have been done, I at least draw the conclusion that the results were not favorable and therefore buried, like happen with far too many study results that do not support assumptions or intended promotions.
Why ? LDL is a repair substance in the body and by reducing LDL repair of blood vessel, naturally the scab bodily repairs cause before they are healed out is also reduced. By moderating repair by reducing the repair substance – LDL – less repair and less scab naturally follows, the priciple of statins. But real needs like “real leakages” of blood vessels and and thinned blood vessels will then also get less repairs which can result in that a small drip is allowed to progress to full scale hemorrhages.
When it happen in the brain it is called a stroke. The real problem that statins do nothing at all to solve is arterial inflammation, which has been shown to be caused of too high bloodsugar, including blood sugar spikes after meals.
The final nail in the coffin for statins comes now: Statins are known and accepted to RAISE blood sugar!
Arterial plaque has even been reversed through reduction of blood sugar spikes.
John Walker,
AD research is already deep into the rabbit hole and finding that the blockade of Mevalonic acid and some of the sub components of that pathway are showing great promise in this area or so they say. So, another feather in the Statin arrow.
Where the arrow gets aimed next is only limited by regulation and ethical constraints.
One Glimmer in that research is the acknowledgement that statins are working by they anti inflammatory effect.
You see where this is going, patents end and another target is required else board rooms shall be requiring some of their own medication to forget about the dropping income from their poster child.
@ sten bsell,
Good comment!
Can I ask what about ApoB/ApoA have been established as being atherogenic by by what pathway? This interests me.
Also are ApoA/ApoB in any way related to Lp(a)?
I too suspect degrading blood sugar control that seems to accompany the advance of years and the corresponding rise in insulin has a place in the causal chain but I’m not so far on with the ‘links’ as you are. How has blood sugar and/or insulin been shown to be atherogenic (you mention inflammation) but what leading peer reviewed papers would you cite as lending the clearest explanation of this?
Cholestane triol was amongst the first biochemical compounds that was demonstrated to induce atherosclerosis in rabbits as far back as 1913 — though the distinction between cholestane triol and cholesterol was not described in Rudy Virchows write-up. We had to wait until experiments conducted on several species to learn of the distinction between cholestane triol and cholesterol, learning at the same time that cholesterol in the pure form is not atherogenic. That development dates to the 1970s. It was about the same time one Dr Kilmer McCully, a pathologist, noted something and promoted a hypothesis around homocysteine which also appears to be strikingly atherogenic.
Can these alternate physiological factors be linked in anyway? Are they each links in one causal chain and do they represent a point of convergence for the generally well accepted life-style risk factors that the medical profession love to remind us of? (Stress, diet, smoking etc.) Or do they feature in independent causal pathways of their own? Does convergence of causes and effect arise much closer to the cells of the endothelium, or is there no point of convergence at all and are the pathways several and completely independent?
I think the answer is out there as the overlooked detail of a huge mass of write-ups so a forensic approach could return it. Would you agree?
Reply to: Chris 16 December 2013 at 12:34 pm #
Thanks Chris.
Since rabbits are herbivores – really grass eaters – the rabbit experiment should have been
discarderd immediately in 1913.
If you follow this link : http://www.trackyourplaque.com/library/fl_04-022postprandialcarbs.asp
a good background for clinical plaque reduction is given.
The other side is the inflammation that can be found more links to by googling NFAT, osteopontin. Here is citation from one: “Large clinical trials have identified hyperglycemia as a risk factor in the development of diabetic vascular complications.”
From Davies summary it seems that the inflammations are dose proportional which means they start earlier, or reversal will not take place until well below some not well known threshold. The crucial thing is however that on a SAD diet postprandial blood sugar often reaches over 7 and 9 for sometimes an hour which reaches into diabetic hyperglycemia, although not that extended.
http://www.fasebj.org/cgi/content/meeting_abstract/24/1_MeetingAbstracts/980.4
I remember seeing an article recently that said the risk of strokes went up when a person discontinued taking a statin. I assumed it was a study from the drug companies who wanted to counteract the recent bad publicity and scare people into staying on their drugs even if they wanted to stop them. Do you know if there was any validity to the study? My husband has been on a statin for almost 20 years and I’ve tried to convince him (and his doctor) that he should get off them, but I don’t want to provoke a stroke. He eats a low-carb diet in spite of the instructions about taking Lipitor, but of course it isn’t very effective since the statin counteracts the benefit of the diet.
The limited benefits of statins, which are unrelated to cholesterol levels, are anti-inflammatory, plaque-stabilizing properties which have a slight benefit in coronary artery disease.
Linoleic acid (LA) appears to be the most pro-inflammatory and atherogenic fatty acid and causes endothelial cell activation and dysfunction which leads to atherosclerosis.
During the past century intake of LA has increased from 2% to 7% of calorie intake in part due the unfortunate dietary recommendations to substitute vegetable oils for animal fats. LA is the direct precursor to the bio-active oxidized LA metabolites (OXLAMS) which have been linked to increased atherosclerosis.
Oxidized LDL plays a far more important role in the progression of atherosclerosis than native LDL.
I find it amusing (and interesting) that cholesterol has been found to attenuate LA induced endothelial cell activation thereby reducing inflammation. (PMID 12701065)
Decreasing intake of omega-6 LA and increased intake of omega-3 fats will decrease inflammation thereby decrease Ox-LDL and CHD risk.
LA is the precursor to omega-6 arachidonic acid which is the backbone of eicosenoids (signalling molecules) called endocannabinoids which acitvate the same receptors that are activated by marijuana.(Hence the name derived from endogenous endocannabinoid)
Increased dietary LA increases AA-derived endocannabinoids which predisposes mice to ectopic lipid storage (belly fat) and hepatic insulin resistance.by centrally mediated hypothyroidism. (PMID 22912402) In other words, increased LA intake interferes with thyroid function which reduces metabolism thereby reducing energy expenditure which results in increased conversion of carbohydrates to fats (in order to prevent elevated blood glucose) which induces obesity, fatty liver and insulin resistance all of which increase CHD risk. (Note:Animals raised for food production are fed grain high in LA to make them gain weight by reducing energy expenditure.)
Reducing LA intake will reduce CHD risk by reducing inflammation and by reducing risk of obesity and insulin resistance. A low carb diet (20 to 30% of calories) will facilitate reducing LA intake as much of the LA comes from snack foods. This is a much better and safer option than statins.
Reply to: J. Cameron 17 December 2013 at 1:03 am #
Great information and comparisons! Can you add some references about the LA and how it can become part of LDL and thereby promote faster oxidation of LDL, or similar?
What about us that have carried excess visceral fat for many years and already have reduced carbs to less than 10% but still suffer dawn syndrome, still far from being diabetic? I was 75 kg up to age 45, then peaked at 97kgs at 65 after I stopped smoking at age 48 and 59.
Now I am back down at 87 and it is very hard to get rid of those last 5-10 kgs, which are largely abdominal or visceral fat . I have the notion that this fat is “old” as it has been there “too long” and whatever exchanges take place are not 100%. What you mention about omega-6 is very interesting. I used to be a “cookie monster” if there was something around I tanked up very well on it knowing nothing of transfats or omega-6 for until after I got ill with angina. To now remove this bad hormone producing fat is probably a nightmare for my system -stored toxins ? – so when the weight drops near to just touch those stores, some silent strike takes place…
It seem if I then try again 6 months later it goes down another tad, then hitting a new wall. Too slow for me now… (…I want it all, I want it now…)
What about adiponectin, could that speed up the lipolysis ? Helped by niacin for instance?
Or what ways have we “to move” this fat, without starvation? Strength training, interval training of course, I know… Anything else?
I for one believe the dawn syndrome is mainly related to remaining insulin resistance as high morning blood sugar is mainly a diabetic issue = poor blood sugar regulation. So called “physiological insulin resistance” seem an illogical function as we can go very well on BS down to 3 with ketones. So how to shed that fat, once ! It is put back by means of sugar which we do not touch anymore so it will be just a one time investment, that I plan for next year. All help appreciated!
sten bsell,
I have a file on most of the studies mentioned but will only send links to those related to overweight.
Increased oxidized omega-6 LA metabolites (OXLAMS) that result from excessive intake of LA are not related to overweight but are related to oxidized LDL and, according to one recent study can be the cause of frequent headaches in some people. In a trial, reducing LA intake to less than 2% of calories reduced headache frequency and duration.
Polyunsaturated fats, which consist of omega-3 and omega-6 fats, are called essential fatty acids because the body can not make them as it does other fats. Animals, including humans,get rudimentary omega-3 and omega-6 fats from grass and other plants and convert these fats to long chain omega-3 and omega-6 “highly unsaturated fatty acids ” HUFA. which are essential for many physiological functions including or brain structure and function. Both omega-3 and omega-6 fats are precursors to eicosenoids which are signalling molecules that control almost all functions of the body. There are about a dozen kinds of eicosenoids each with a number of subtypes. The latest eicosenoid to be discovered are endocannabinoids which activate the same receptors activated by marijuana and control many functions including appetite, metabolism, learning and memory. Like to much pot, increased LA intake elvates endocannaboids can cause increased appetite, decreased metabolism and memory loss.
LA is the precursor to arachidonic acid (AA) which is the backbone of endocannabinoids including 2-AG and anandamide.. When intake of omega-6 LA is excessive, the body can not compensate by making more omega-3 so, eicosenoids get out of balance and screw up a lot of physiological function.
A recent study compared the increase in obesity between 1909 and 1999 with changes in food consumption of over 270 different foods evaluated , only those high in LA were strongly associated with increased obesity (soybean oil, chicken and shortening.) (Sugar was weakly associated with obesity.)The major part of this study, Dietary Linoleic-Acid Elevatates Endogenous 2-AG and Anandamide (which are endocannabinoids) and Induces Obesity, concerns trials regarding the effect of increased LA intake on rats.. (PMID 22334255) The study has a few fundamental errors but the finding that increased LA intake causes obesity is sound.
I have been trying to wrap my head around the subject of endocannabinoids since the above study came out and have accumulated a lot of studies which explain some of which is not explained in the above study.
The endocannabinoid (EC) system consists of the two most studied endocannabinoids are 2-AG and anandamide., the receptors CB1 and CB2, and the enzymes that synthesize and degrade the ECs.
Note that if the EC receptors are blocked, mice do not become obese.
The enzyme that degrades anandamide is FAAH while 2-AG is degraded by MAGL. Because the ECs are degraded, the impact if elevated ECs is muted compared to pot. If the degrading enzymes are inhibited, the levels of endocannabinoids from LA can rise and make a mouse stoned just like pot does.
People with genetically impaired FAAH which degrades anandamide tend to be overweight because the ECs are not fully degraded. Mice become obese if EC degrading enzymes are blocked.
When obesity is induced in mice by increased ECs, the activity of FAAH that degrades anandamide is increased whereas activity of MAGL that degrades the EC 2-AG does not increase. As a consequence, mice and humans that are obese tend to have elevated levels of the EC 2-AG which will tend to increase appetite and decrease energy expenditure. This seems to be the reason that once a person gets overweight it is difficult to lose weight. Metabolism actually decreases when ECs are elevated. Patience is required, I think.
Omega-3 fats have anti-obesity functions. Omega-3 fats increase oxidation of lipids and decrease the conversion of carbohydrates to lipids. The anti-obesity characteristics of omega-3 fats are abrogated by excessive intake of omega-6 fats and excessive intake of high glycemic foods. I will send a link on this subject in another post.
Since you have a very low carbohydrate diet you have probably already greatly reduced your intake of n-6 LA, much of which comes from snack foods, bakery good, french fries etc. I recommend reducing LA intake as much as possible and getting some omega-3 from fish or supplements.
A century ago animal foods provided people with a fair amount of omega-3 fats but the practice of grain feeding animals has resulted in a reduction of both short chain and long chain n-3 fats in foods from animals.
For Stan
I read in your post “when the weight drops near to touch those stores, some silent strike takes place.” Does that mean that you suffer a ‘lapse’ in your eating habits? Also I wonder about “it seems if I then try again 6 months later…..it hits a wall.”
In my experience, sticking steadfastly to a (very) low carb day in and day out will steadily and permanently reduce those stubborn fat stores to acceptable levels. It’s not easy though. Our culture is EXTREMELY carb orientated and temptation is everywhere, absolutely everywhere and with Christmas, the great eating and drinking fest, upon us with everyone tucking into mince pies, etc. it’s hard to get excited by a chunk of cheese and a handful of walnuts, nice as they are.
I’m afraid you just have to be tough with yourself, Stan. Don’t be discouraged and it will happen. If I can survive without breakfast cereals (did I really eat those?) rice, pasta, all but tiny amounts of toast – 2/3oz with my breakfast eggs – ANYONE can.
Sten.
‘Lights Out’ would be recommended reading for understanding how cortisol may command metabolic dynamism.
Increased prospects of gluconeogeneis (conversion of proteins to glucose under the influence of elevated cortisol) would be a curiosity that may deliver answers.
I noticed and wondered for a while why I could sense a rush following ingestion of protein. i imagine I have ‘aggressive digestion’ with ingested contents being passed over the GI divide too quickly.
Fat and fibre in chyme (ingested contents of the stomach) compare with the control rods in a nuclear reactor. So the way to attenuate aggressive digestion and prevent cabs, (and proteins under the influence of cortisol if it high) from delivering a significant spike in postprandial BG and insulin.
If visceral fat is not decreasing then:
Insulin could be high because pressure on BG and BG itself may be high.
Insulin resistance may impede efficacy of measures taken to reduce visceral fat
Cortisol may be high.
The protein presence in a low carb regime may be resulting in gluconeogenisis.
There may not be adequate balance of fats in the diet.
There may not be adequate measures of soluble fibre in the diet.
Maybe vitamins and minerals in the diet are not achieving the right status and not resulting in the rightful efficacy as co-factors in metabolism.
I suspect, and I have no real evidence, that supplementation with B vitamins helps defeat insulin resistance and so often I feel more energised after taking B vits. Dr Moses Suzman routinely dispensed B vits to the diabetics amongst his patients.
There is no doubt lipolysis and ketosis is natures way of capitalising upon sequestered body-fats to delver evolutionary advantage when food and sugars are short, but the dietary modifications to induce lipolysis and ketosis may alter things which challenges supply of certain antioxidants. Perhaps we should not encourage weight loss to be too rapid. ketosis to be too intense, and maybe it is reasonable to ease back from time to time.
High fat diets that encourage lipolysis and ketosis and that don’t look to supply adequate amounts of soluble fibre and pectins may result that our symbiotic and friendly bacteria in our guts are not producing the waste products that result when they feed off fibre — and that have beneficial influences upon our well-being.
Sten Bsell,
I entered a lengthy reply to you comment last night mainly regarding endocannabinoids and obesity that has yet to be posted. Perhaps it was too long. Maybe it will be posted later, maybe not.The subject of endocannabinoids is very complex and seems to be avoided by most bloggers.
I don’t think adiponectin or niacin would have any effect on weight.
Your 10% intake of carbs is, of course a ketogenic diet. According the “The Perfect Health Diet by the Jaminets, the body can utilize about 20 to 25% of caloric intake as carbs and carb intake in excess of that amount is converted to lipids. So a diet with 20 to 30% of calories a carbs will not significantly effect lipogenesis and weight gain. The jaminets advocate a diet with about 15% protein, 20% carbs and 65% fat. I don’t count carbs but my diet is very high fat and probably approximates the the diet advocates by the Jaminets.
Dr. Michael Eades advocates a ketogenic diet in his book “Protein Power”. I have not read the book but have read the reviews on Amazon and note that many people have had great success with the diet while others have had not had success in spite of concerted effort. Perhaps you are one of those who does not do well and a ketogenic diet.
Dairy and eggs probably provide about half of my calories. Most of the dairy products I eat are made from raw milk from pastured cows. I eat a lot of aged raw milk cheese in part because of the high vitamin K2 content. Cheese can be legally shipped across the state line in the U.S. as long as it is aged for 30 days or more. I get raw milk cheese and butter from Amish farms in Pennsylvania. Raw milk for human consumption is illegal where I live so I buy raw milk “for pet consumption” that is produced by a local farm I also get organic eggs from pastured chickens (They are hard to come by and expensive.) I mention this because the dairy and eggs from pastured animals contains more than three times as much long chain omega-3 fats (EPA and DHA) as dairy from grain fed animals.. A century ago the dairy and eggs provided most of the omega- 3 HUFA (EPA and DHA) in the average diet and people seemed to fair quite well.
Dairy products have a lot of calcium but are short on magnesium so if a person eats a lot of dairy as I do it is almost important to take magnesium supplements.
We avoid all vegetable oils that contain a lot of LA. We avoid fried foods and limit poultry to skinless chicken breast which have low LA content.
These are some of the things we do to avoid excessive LA intake and get adequate omega-3 fats.
Janet B.
Your response is just what I needed to read this morning.
I am in London for a week’s holiday. We are surrounded by poor quality food, and that includes the processed stuff marketed by the posh shops ( I read labels! ).
I am preparing protein/high fat salads in my hotel room, and eating “al fresco” in the fairly decent weather for this time of year.
I am having coffee in only those coffee houses which serve double cream ( few and far between), and taking a portion controlled amount of quality chocolate and shelled walnuts into the theatres for the intermission treat, so that I don’t feel deprived.
It had taken me the best part of a year to reach this stage of my Low carb, high fat regime, having hit some snags on the way, especially wihen socialising, so, it makes sense to be really strict on myself when I am left to my own devises. The outcome is worth it, with increased health and energy being abundant.
I don’t even try to explain myself to those who counter me with “how boring!”, because it is neither boring or unhealthy, and I NEVER feel hungry, which is the main devil of temptation.
Like most people, I need a spot of encouragement to keep me on the straight and narrow, and your comments have done just the trick for me today. Thankyou.
Jennifer
…and may I suggest 85% Dominican Republic chocolate with a handful of skin-on almonds? Total luxury and extremely satisfying. Better than any over-sweetened commercially produced “snack”
Janet, I have finally made it to 85% choccy….I am amazed at how my taste buds have adapted, and it is a lovely feeling. I want the goodness from cocoa, with minimal sugar, and I will work towards 90%! Ho! Ho,
I have implemented an even stricter low carb regime since early January, and feel good, but with minimal weight loss, which is not important. The health benefits are exceptional, and I do get such help from contributors on these sites.