Familial Hypercholesterolemia (FH)

While I was in South Africa, at the Professor Tim Noakes hearing, Familial Hypercholesterolemia (FH) came up both home and away. Back in the UK, a study was published by the Queen Mary University of London arguing that public health agencies should routinely test the cholesterol levels of infants (aged one to two years) alongside the administration of childhood vaccinations. The university’s article on the paper can be seen here. The journal paper can be seen here – not on open view, but I’ve got the full PDF.

At the Noakes hearing, FH was raised by the prosecution as an argument as to why cholesterol is harmful. The argument goes – people with FH have higher heart disease and high cholesterol and therefore high cholesterol causes heart disease. (At the risk of closing the debate before having it, Dr Malcolm Kendrick dismisses this logic as follows: People who smoke have higher lung cancer and yellow fingers. Do yellow fingers cause lung cancer?!)

Let’s unpack the very interesting condition that is Familial Hypercholesterolemia (FH)…

Lipoproteins

We need a basic lesson in lipoproteins to understand Familial Hypercholesterolemia (FH).

Lipoproteins are microscopic bodies found in our blood stream. We can think of lipoproteins as tiny ‘taxi cabs’ travelling round the blood stream acting as transporters. They are needed because the vital substances fat and cholesterol are not water soluble, so they cannot exist freely in blood. The lipoproteins, therefore, carry fat and cholesterol around the body to perform their critical tasks.

There are five different lipoproteins. The largest lipoproteins are called chylomicrons. It would be logical for them to be called extremely low density lipoproteins (ELDL’s), but they aren’t. The next largest are very low density lipoproteins (VLDL’s), which are often called triglycerides, also somewhat unhelpfully. There is a lipoprotein called intermediate density lipoprotein (IDL), which you’ve probably never heard of. Then we have the much more widely known low density lipoprotein (LDL), erroneously known as ‘bad’ cholesterol and high density lipoprotein (HDL), equally erroneously known as ’good’ cholesterol.

If one chylomicron lipoprotein were the size of a football, then one VLDL would be about the size of a large orange, one IDL would be about the size of an apricot, one LDL about the size of a plum and one HDL about the size of a small grape. You can see where the notion of density comes from – the smaller the lipoprotein, the more dense/tightly packed the contents and hence the smallest lipoprotein (HDL) is high density and the largest lipoprotein (chylomicron) is the one that should, logically, be called extremely low density lipoprotein. (Ref 1)

Familial Hypercholesterolemia (FH)

FH is a genetic condition caused by a gene defect on chromosome 19. The defect impairs the body’s ability to remove low density lipoproteins (LDL) from the blood stream, resulting in consistently high levels of LDL. There are two types of FH: Heterozygous FH is found in 1 in 500 people; Homozygous FH is much rarer, occurring in 1 in a million births. (Ref 1)

Human cells have LDL receptors, so that they can receive LDLs from the blood stream and let them into the cell with all the vital lipids that they contain. With Heterozygous FH, the LDL receptor works to a slight extent and some vital lipids will get through to the cell. With Homozygous FH, the LDL receptor doesn’t work at all and so the cell doesn’t get the lipids that it needs.

Please keep in mind from the outset how rare even the milder form of FH is – 1 in 500 people. Judging from the comments on my blogs, however, you would think that maybe 1 in 10 people have FH – some doctors are clearly telling people that they have FH simply because they have a higher than average blood cholesterol level. (PCSK9s are currently only approved in the UK for FH – I suspect this is why more and more people are being told that they have FH). My first tip to anyone told they have FH, therefore, is to have a proper genetic test for the condition – a cholesterol level of 9, for example, is quite normal as defined by the normal distribution. A genetic chromosome defect is something quite distinct.

The classic view of FH

The classic view of FH is framed by the widespread assumption that blood cholesterol levels are a marker of heart disease. As this post shows, there is a relationship between blood cholesterol levels and all-cause mortality and cardiovascular disease (CVD) mortality – in men and women – but it is inverse i.e. the higher the cholesterol level, the lower the death rate and the lower the cholesterol level, the higher the death rate. That’s for 192 countries for which the World Health Organisation (WHO) has data. That’s a slightly inconvenient truth.

The classic view of FH argues that people with FH have higher heart disease and high cholesterol and therefore high cholesterol causes heart disease. Does the evidence support this view?

Because of the rarity of FH, data are not abundant. Most data emanate from the Simon Broome Register Group, which started to study patients with Heterozygous FH (the 1 in 500 form) in 1980. (The Simon Broome Register Group has been funded by Astra Zeneca, Pfizer and Merck Sharpe and Dohme, by the way).

One of the first publications from the Simon Broome Register Group dates back to 1991. This review analysed standardised mortality ratios (SMR) for 282 men and 244 women aged 20-74 with Heterozygous FH. The participants were followed up for 2,234 person years. The results were that the highest SMRs, relative to the non-FH population, were for the age group 20-39 and the higher death rates for FH sufferers decreased significantly with age, such that mortality was no higher for people aged 60-74 with FH than for people of the same age without FH.

This widely referenced study also derived from the Simon Broome Register Group. It followed 2,871 patients with Heterozygous FH who were recruited from 21 outpatient lipid clinics in the UK from 1980 to 1998. The patients were followed for 22,992 person years. The standardised mortality ratio (SMR) was calculated for these patients and compared with death rates in the non-FH population in England and Wales. There were 169 deaths recorded, including 102 from coronary heart disease (CHD) and 32 from cancer. The SMR for CHD was 2.5 times higher for the FH sufferers than the general population, but the all-cause death rate was no higher. Non-CHD mortality was significantly lower in men and women. The study found that patients with Heterozygous FH were dying more of CHD, but less from cancer and thus the death rate was no higher overall.

The combined findings from these two Simon Broome Register Group papers show that, if you genuinely have FH and you are aged 60 or over you should be pleased to know that you have a lower risk of cancer and no greater risk of heart disease. If you have FH and are aged 39 or higher, you are already past the highest risk period of your life for heart disease. Even in the 20-39 age group, there were 6 deaths in 774 person years studied – less than a 1 in 100 incident rate and that’s in 1 in 500 people.

Another widely referenced, long, Dutch, study set out to estimate all-cause mortality from untreated FH. The study was described as a “Family Tree Mortality Study”. It traced back numerous descendents from a single pair of ancestors in the 19th century. Those with a probability of carrying the FH mutation were followed. This involved 250 people analysed for 6,950 person years during which time 70 deaths occurred. The study found that mortality was no higher in carriers of the FH mutation during the 19th and early 20th century. Mortality rose after 1915, peaked between 1935 and 1964 and fell thereafter. Mortality also differed significantly between the branches of the descendents studied. The conclusion was that the risk of death differed too much over time, and too much between different descendents, to support the view that high cholesterol was the factor. The study concluded that environmental factors must play a part and must be researched more thoroughly. Sadly this has not happened, because the cholesterol hypothesis has become the only factor considered important with FH.

An alternative view of FH                                                                                 

If you are not limited by the assumption that high cholesterol is bad, you can view FH quite differently.

My logical consideration of FH suggests to me that the problem is that the LDL receptors don’t work properly and therefore LDLs cannot get into the body’s cells in the way that they are supposed to. This means that cells don’t get the vital LDL, carrying the vital protein, lipids and cholesterol needed for the cell’s health. LDL in the blood stream is high because the LDL has stayed in the blood stream and has not been able to get into the cells – where it is supposed to go. Hence high LDL blood levels are the sign that someone has FH. The high LDL levels are, however, a symptom and not a cause, or a problem per se. The problem is that the health of every cell is compromised by LDL not getting into those cells. This includes heart, brain and muscle cells – all cells. Someone with FH can therefore have heart problems – because of too little LDL reaching the heart cells – not because of too much LDL in the blood stream. How differently things can be seen when one is not blinded by thinking that cholesterol or lipoproteins are bad.

The heart disease/cancer evidence supports this hypothesis. If the vital substances in LDL cannot get to heart cells, heart disease would be more likely. If the vital substances in LDL cannot get into a cell that has become cancerous, that cell can’t be fed and the cancer is less likely to spread.

A genetic view of FH

There are also alternative hypotheses for FH involving genetics more broadly. These make complete sense. This article, cited almost 50 times, studied 1,940 FH patients for 65 polymorphisms (different forms) in 36 different genes and found a significant association between “Prothrombin G20210A” and CVD risk. Don’t worry about the unfamiliar words – all we need to know is that Prothrombin G20210A is a human gene mutation that increases the risk of blood clots. The study found, therefore, that people with FH who had an accompanying genetic mutation that increased blood clots were more likely to suffer CVD. That makes sense, of course. It also makes sense that a genetic defect, which is what FH is, has more than one consequence. Another genetic consequence of FH (completely unrelated to cholesterol) can be increasing the risk of heart disease (and the same genetic consequence or a different one may be reducing the risk of cancer). The raised LDL would, again, be a symptom and not a cause of heart disease in any way.

What about statins?

You may be interested to know that there are no intervention studies that directly show mortality benefit of cholesterol lowering in FH. Despite this, because of the limiting belief that cholesterol is the problem (and not the symptom), all treatment for FH focuses on lowering cholesterol. Statins are administered. Bile acid sequestrants are used (e.g. cholestramine). Ezetimibe might also be used, which inhibits cholesterol absorption in the gut. Anything and everything that can lower cholesterol is considered part of the toolkit. No benefit has been established in doing this and yet the Queen Mary university article, recommending routine cholesterol testing of infants, proposes that statin ‘therapy’ can start earlier. This recommendation could lead to children being put on statins and other cholesterol lowering medication during their most formative years when we know that cholesterol is a vital component in cell and human development. A clearer case of child abuse would be difficult to find. (The lead author of this infant/statin paper, David Wald, is the founder and shareholder of Polypill Ltd – a four in one drug, which includes a statin).

If raised LDL is a symptom and not the problem, any cholesterol lowering medication would only make things worse. If LDL not getting to cells is the real harm of FH, then any attempts to lower cholesterol will make things worse. We know from the brilliant book by the Yosephs that cells will try to produce cholesterol if they cannot get it from the blood stream. We also know that brain cells produce cholesterol because of the blood brain barrier (which is why statins can have particularly harmful effects to mind, memory and mood). If people with FH are already suffering from LDL not getting to cells, then impairing the cell’s ability to make cholesterol will make things even worse.

People with FH should ideally be given medication (if anything existed) to stimulate cholesterol production within the cell, so that the cell would at least get the vital cholesterol it needs, even when it couldn’t get it from the blood stream.

How differently problems can be viewed when unconstrained by limiting beliefs.

p.s. if you would like to see the Dr Malcolm Kendrick yellow finger hypothesis and a five minute take down of FH, watch this from 15-20 mins.

Ref 1: Mangiapane EH, Salter AM. Diet, Lipoproteins, and Coronary Heart Disease: A Biochemical Perspective: Nottingham University Press 1999 January 1, 1999.

27 thoughts on “Familial Hypercholesterolemia (FH)

  • avatar
    February 17, 2017 at 8:02 pm
    Permalink

    Hi I recently had a lipid panel done and everything has changed, gone up, the Dr is thinking about putting me on Statins but i am going to refuse. My mother, sister have high cholesterol. I was diagnosed with CLL last April and have had Dr. appts here , there and everywhere, biopsies etc. The last 6 months have been very stressful for me. Prior to that i was pretty much stress free and living the good life. My question is do you think stress can play a role in high cholesterol ? I have also been on a raw veggie diet the last 6 months , could that also effect the counts? Thank you

    Reply
    • avatar
      February 18, 2017 at 9:31 am
      Permalink

      Hi Peggy
      I’m really sorry to hear of all the things you’ve been going through and the stress this has understandably put you under.

      You may find my main post on cholesterol and statins interesting (http://www.zoeharcombe.com/2015/03/worried-about-cholesterol-andor-statins/)

      The short answer to your question – can stress play a role in (high) cholesterol? Absolutely. Even the stress of the appointment affects the results – one of the links from that main post shares the inaccuracy of the test (19% for starters!)

      I’m personally not sure about a raw veggie diet – especially when fighting serious illness. A number of nutrients are only found in foods of animal origin and meat/fish/eggs/dairy are nutrient dense (http://www.zoeharcombe.com/2014/04/healthy-whole-grains-really/) Cutting out junk is a great idea, but not cutting out highly nutritious foods.

      All the best for your appointments
      Best wishes – Zoe

      Reply
  • avatar
    January 20, 2017 at 1:00 pm
    Permalink

    HI Zoe,

    I am 42 have been diagnosed with high cholesterol at total 7.2 on average for the last 2 years. I had a test for FH which came back negative. Just recently I had another test and it shot up to total 8.6, but LDL 6.2, TRI 1.4 and HDL 1.7. I am tall and not overweight.
    I discussed this with my Cardiologist who said that I have FH, I told him about the test I had that was negative, but he seemed convinced that I have it, citing that there is probably another gene I have that has not been discovered yet, and says I should get a CT calcium score done, and probably be on statins or injection statins.
    My mum and dad both have high cholesterol and are on statins, but they are both still around thankfully and in their 70s. My dad recently had a bypass at 72 though. I’d be interested to know if you think i should get a second opinion?

    Reply
    • avatar
      January 20, 2017 at 2:49 pm
      Permalink

      Hi Tim
      I actually gasped out loud when I read the bit about the gene that’s not been discovered yet. WTF?! How can a so-called professional bare faced make up something like that?!

      The injection statins comment make sense. It explains this person’s (I can’t bring myself to call him a doctor) enthusiasm to ensure that you have FH (when you clearly don’t – by having a completely normal chol level and/or by genetic confirmation). At the moment, the wildly lucrative drugs (with largely unknown consequences) are only allowed for those with FH. Check this out: http://www.zoeharcombe.com/2016/04/pcsk9-inhibitors-statins/

      You may also find this interesting (http://www.zoeharcombe.com/2015/03/worried-about-cholesterol-andor-statins/) Ideally, you would never have ‘got into the system’ but, given that you have, – check out the link from this post that goes to the post about “normal”. You are as normal as chol is (when they don’t statinate).

      Read the leaflet in your parents’ statin meds and read the bit about caution being advised for over 70s being in statins (because chol is even more important for older people – it’s pretty flipping vital for younger people too). Then maybe go and ask your parents’ doc(s) if they have read the leaflet and if so WTF are they doing?!

      If your higher score (still not that high) was recently and you live in the N hemisphere, this will be a reflection of lack of sunshine. Sunbathe sensibly as soon as the nice weather returns and then the body makes vit D from cholesterol – that’s one of the many, many reasons why the body makes cholesterol.

      I’m still in shock at your doc – he should be on a TV prog about con men!
      Best wishes – Zoe

      Reply
      • avatar
        January 20, 2017 at 3:28 pm
        Permalink

        Thanks for the reply Zoe . I read with interest all of your articles about this and to me it makes perfect sense . I am still a bit confused though . Do you know also if having kidney stone and also gum disease is linked to high cholesterol and or Athercolosis ?
        I am now not sure whether to go for the scan or not ? Confused .

        Reply
        • avatar
          January 20, 2017 at 3:47 pm
          Permalink

          Hi again – yes good one – I was so shocked I missed the CT test query!

          My go to person for proper heart disease doc views is this chap (https://drmalcolmkendrick.org/2016/03/22/what-causes-heart-disease-part-x/)
          You’ll enjoy reading his other posts too – this is part X of a series that’s over XX by now – you will probably enjoy them all.

          I would worry more about the guy who makes up genes going anywhere near me again than I’d worry about the CT scan! It looks like it can tell you some interesting things, but it’s by no means definitive. I simply wouldn’t trust gene-make-up-man to be unbiased when sharing the results. I get the impression he wants to try another test to get you on PCSK9s. Do ask him if he is being paid to find patients for this new drug!

          Best wishes – Zoe
          p.s check out this guy’s posts too – he’s worked out how to use fat to drop cholesterol and explains how! http://cholesterolcode.com/how-to-do-the-cholesterol-drop/
          Given that I don’t care about cholesterol, I wouldn’t play any games with it – but this – or sunbathing – could drop cholesterol if you were bothered!

          Reply
  • avatar
    December 22, 2016 at 7:50 am
    Permalink

    Hi Zoe, so much seems familiar in these comments regarding my questions, lack of answers from medicos and questions of how did I get to this condition?
    I’m 59 recently had a heart attack, cardiovascular disease, stent put in and usual recommended treatments of drugs; including statins.
    I had a bad reaction to statin treatment and gave them the flick pretty quickly, much to the disdain of my consultant doc.
    Short version question is… How did I get this plaque build up in my arteries and can I reverse it?
    Yes I have been a smoker, but also a very active person my whole working life with a pretty non diet based eating regime i.e I have been a very fit and active person for a long time and gave up smoking for over 10 years, then bang, complete blockage of left descending thing in / on my heart. Lucky to be here I guess.
    Any comments on how it all got to this and the other drugs I’m on like brilinta, metoprolol,ramipril and aspirin.
    Feeling like a guinea pig
    regards
    Sean

    Reply
  • avatar
    December 8, 2016 at 11:23 pm
    Permalink

    Dr Harcombe,
    Could you please point me in the right direction to study up on high blood pressure (HBP) probably due to high T3 hormone. I need the latter because I had thyroid cancer so I have no thyroid. I am terrified to go to the doctors (with my HBP) because I think he will put me on some god awful blood pressure lowering drug which will cause more problems than I have at the moment. I am also stuck because I know that thyroid medication interferes with blood pressure lowering drugs (they both use the availableTBGs).
    Where do I start Dr H? It took 3 years to get my thyroid meds to an optimal level and ratio, I don’t want to have to do all that again.

    Reply
    • avatar
      December 9, 2016 at 9:14 am
      Permalink

      Hi Lahs
      My first thought would be – do you genuinely have high BP? This may help http://www.zoeharcombe.com/2014/06/diabetes-cholesterol-bp-normal-is-no-longer-normal/
      The true average is about 140/90 and anything on the normal distribution is normal – by definition!

      There’s nothing that jumps out with a quick pub med search (academic articles). This looks interesting and has some good academic refs http://www.medscape.com/viewarticle/733788_1
      I really would be challenging what is considered normal for BP

      You’ll enjoy this just for support/interest https://drmalcolmkendrick.org/2015/05/01/treating-thyroid-patients-like-children/

      One of the best ways of lowering BP quickly if you’re interested is a low carb diet. Any carbs that are not used up by the body (and most people with access to food eat more carbs than they need most days) are stored as glycogen (and then turned to fat) but we can keep a steady glycogen level of about 500g in the body at any one time. For every gram of glycogen, the body holds 4 grams of water. Think of a pressure cooker – more water = more pressure. The body is similar. If you keep your glycogen levels low (anything below 150g of carb a day should help) – your water held is also lower. If you do a very low carb day (nearer 50g of water) you can lose 5lb ‘overnight’ and BP drops noticeably.

      Hope this is of interest
      Best wishes – Zoe

      Reply
  • avatar
    November 14, 2016 at 1:39 pm
    Permalink

    Hi Zoe.
    Thanks so much for putting my mind at rest. Perfect timing. Got my FH results today. Negative.
    Although they say it’s likely I’ve polygenic Hypercholesterolemia.
    My TC after intermittent fasting were 15.9 and 15.8, LDL 12,6, HDL 2.7 Trigs 1.
    This weeks fasted bloods after a meal of chicken and peppers baked in Philadelphia cheese topped with Parmesan were TC 12.6 LDL 8.9 HDL 2.8 and trigs 0.8
    Then consultant said the only time he had seen such high results were in an anorexic. Makes sense. With a bit of tweaking in my diet I’m sure I’ll get there.
    Kind regards
    Annette

    Reply
    • avatar
      November 14, 2016 at 2:27 pm
      Permalink

      Hi Annette – well I’ve never heard of polygenic Hypercholesterolemia before and I suspect it’s a conveniently made up term!

      “This condition is caused by a susceptible genotype aggravated by one or more factors, including atherogenic diet (excessive intake of saturated fat, trans fat, and, to a lesser extent, cholesterol), obesity, and sedentary lifestyle. The involved genes have yet to be discovered.” (http://emedicine.medscape.com/article/121424-overview) I bet they have ho ho!

      This may be of interest (http://www.zoeharcombe.com/2015/03/worried-about-cholesterol-andor-statins/) Especially the link to the Fraser paper showing a 19% difference in chol test readings is pretty much to be expected! (http://www.bmj.com/content/298/6689/1659) The whole thing is a joke

      Best wishes – Zoe

      Reply
      • avatar
        December 18, 2016 at 9:39 pm
        Permalink

        Hi Dr Harcomb,
        This may not be the best way to enter this discussion, but thought you might be interested in my story. I’m 70, have HeFH with LDL alone over 500 mg/dl, yet by Electron Beam Computed Tomography, done 5 times over a decade, my coronary calcium burden is zero. My last stress ultrasound showed my heart to be decades younger than my chronological age. After much searching I finally found a Harvard researcher that seems interested in me (and my similar older sister, who also has HeFH and a low calcium score). I donated a blood sample, but have found out I will probably never hear any results of any investigations. What I find perplexing is the persistent belief that I “must have something that is protective” from the “obviously dangerous effects of elevated lipids”, rather than my idea that I simply don’t have the “something else that causes plaque”. Occam’s razor says to me that a single explanation (absence of plaque forming gene?) is much simpler than a two part explanation (presence of plaque forming gene PLUS presence of plaque protective gene). Only when the single step explanation must be excluded should anyone consider the two step solution.

        Reply
        • avatar
          December 19, 2016 at 7:21 am
          Permalink

          Hi Rwbramel
          Thanks so much for sharing this – quite fascinating!

          I think that’s most unfair that you give bloods and they don’t give the results back! I would make any future help conditional on a return.

          Have you come across this blog? https://drmalcolmkendrick.org/ If you look at the (now over 20) parts of the What really causes heart disease post, you may find many ‘black swans’ that don’t add up and hypotheses that do. Cholesterol per se is protective – it’s just most people are too wrapped up in the diet heart hypothesis to realise this!

          Hopefully my blog was of interest in that, having made it this far, you (and sister) are highly likely to be around for many more years to follow! And with a sharp mind by the looks of it :-)

          Best wishes – Zoe

          Reply
  • avatar
    November 14, 2016 at 12:16 pm
    Permalink

    Hi,
    My husband (62) has recently suffered a couple of attacks of angina. He will be getting a chest x-ray soon just to check it’s not a lung problem.
    He has a cholesterol reading of 8 which is high, this seems paradoxical given that he is not overweight at all, keeps himself very fit, doesn’t smoke, eats a healthy diet with plenty of vegetables etc. I switched him to butter about 5 years ago as up until he and I got together his ex had been buying the flora type stuff and also Elmlea instead of cream! He hardly eats any dairy apart from cheese. He doesn’t eat desserts and I also got him to stop putting sugar in tea (he still has it in coffee) and to cut down massively on biscuits (now one a day).
    It’s such a shock for us to find someone as fit as he is suddenly finding it a struggle to complete 7 lengths of the pool non-stop when he had previously been quite easily managing 50. When I say he is fit he has a BMI of 23, he is on his rowing machine for 30 minutes a day. He has never smoked and drinks very moderately – i.e. nurses half a pint in the time it takes the rest of the group down a couple of pints.
    His father had a heart attack at 49 so we are wondering if it is FH.
    I know you cannot possibly give a diagnosis or any medical advice in this setting. But I would be interested in hearing your thoughts on what investigations we ought to seek.

    Reply
    • avatar
      November 14, 2016 at 12:26 pm
      Permalink

      Hi Frances
      I’d be astonished if a reading of 8 were indicative of FH. There can be other hereditary heart conditions not connected to FH (indeed, given the rarity of FH, other factors are more likely).

      It seems like you’re doing the right thing getting this checked out urgently (I hope your appointment is v soon?) Angina can be confused with heartburn but anything that seems like chest pain requires immediate attention. The “struggling to swim 7 lengths when 50 previously was easy” is worrying. There may be circulatory issue with such breathlessness. There could also be other reasons for this e.g. panic attacks/extreme anxiety for some reason – but this all needs urgent medical examination.

      I can’t advise but I would suggest getting to a doc pronto!

      Best wishes – Zoe

      Reply
      • avatar
        November 15, 2016 at 5:02 pm
        Permalink

        Thank you very much for your reply Zoe. It is very worrying. I am concerned it may be something to do with living in a house that is only heated by wood burning stoves and old ones at that. He has been put on the waiting list for an angiogram but there is a wait of 24 weeks!
        Thanks again for the reply.

        Reply
        • avatar
          November 15, 2016 at 5:48 pm
          Permalink

          Hi again – I thought about something more reassuring – hopefully father had other risk factors that hubby doesn’t? smoking? sedentary lifestyle? risky job? exposure to something? We don’t inherit everything!
          Good luck with everything
          Best wishes – Zoe

          Reply
  • avatar
    November 10, 2016 at 6:37 am
    Permalink

    Hi Zoe, I have FH which my mum, brother and I all have. We think my mothers father may have had it, as had heart disease and died of a heart attack. My gp referred me to an endocrinologist at the hospital. They tried me on every statin going and I had terrible side effects and the main one being muscle problems that made me feel like an old man.

    So, I couldn’t tolerate any statin on the market. They then tried me on Ezetimibe with again, terrible side effects which I couldn’t tolerate. They ended up putting me on Omacor ( an oil capsule). I take two a day and this keeps my tryglicerides at a lower level. Unfortunately, the medical profession at times have not updated themselves with the latest research and they even at one point told me not to eat eggs !!!!

    Do you know if the Omacor is sufficient for me, or should I be taking anything else to take to stimulate the cholesterol and if so, where would I get this from, as I know for certain my gp won’t give me this.

    (I’m loving the diet and have lost 12 pounds of weight in the first two weeks and really enjoying and sticking to phase 2).

    Reply
    • avatar
      November 10, 2016 at 8:51 am
      Permalink

      Hi Michael – huge congrats on your weight loss and good to hear you’re enjoying how you’re eating :-)

      I can’t advise on any personal health issue – I’m sorry to hear you’ve had such bad experiences with attempts to lower cholesterol (but not surprised) – this FH article may offer an explanation. If you genuinely have FH (genetic defect confirmed, not presumed), your cells will already be suffering from low LDL – statins would make this worse.

      This article explores statins and cholesterol more widely and may be of interest http://www.zoeharcombe.com/2015/03/worried-about-cholesterol-andor-statins/

      Avoiding carbs lowers triglycerides interestingly enough – so more fat meals and fewer carb meals in Phase 2 and your triglycerides may go lower still.

      I don’t think there is anything that stimulates cholesterol production and, you’re right, it would unlikely ever be prescribed! My personal view is just leave the body’s brilliant, incredible cholesterol mechanism alone and it will do what it can do. With genuine FH people, it is impaired, but the body’s ability to adapt is also incredible.

      Let’s hope your body is adapting as well as your mind!

      Best wishes – Zoe

      Reply
      • avatar
        November 20, 2016 at 1:12 pm
        Permalink

        Hi Zoe, I just wanted to say a big, big thank you to you and your husband. I have been on the diet for three weeks and have lost 19 pounds in weight. The main thing is that I discovered that I had a serious problem with yeast and candida and had really bad candida die-off in the first two weeks. I kept on phase 2 and then had some wholemeal bread without sugar, made in our bread machine.

        The day after my symptoms returned and it also has when I have had a glass of wine. It appears to be a yeast intolerance, linked to candida. I realise now that I had been suffering for years with leaky gut, chronic fatigue and related inflammatory health problems. I have also suffered with anxiety all my life and the information I have read, links anxiety and depression (again which I have had a few times) to candida and yeast intolerance.

        The good news is that I have so much more energy, feel good, am sleeping for 7 hours a night compared to 12 and 13 hours I sometimes used to sleep. So, thank you once again and this is an eating plan for life for me now and it has turned my life around completely. :)

        Reply
        • avatar
          November 20, 2016 at 1:57 pm
          Permalink

          Hi Michael
          Thanks so much for letting us know! It’s so lovely to get an update like this. We’re so pleased that this has helped you.

          It’s a bit tough when there are things that are no longer able to be tolerated, but best to know and then decisions can be made. Andy is fine with wine but tends to suffer quickly and badly with beer, so he has a choice. He’s at the match (Wales SA) next weekend, so he may well have a beer – but he knows what will happen so he also might not!

          Great to hear about the energy and sleep too – keep up the fab work!
          Best wishes – Zoe & Andy

          Reply
  • avatar
    November 8, 2016 at 1:18 pm
    Permalink

    Hi Zoe,
    I just want to say thank you for these very interesting posts.
    My mom showed me an article in the Telegraph about paper you linked above about giving statins to babies and I think i screamed out loud! – especially now as a new Dad.
    Unfortunately I believe it will take a generation to change people’s mindset about cholesterol especially when you have to declare having ‘high cholesterol’ when getting life insurance!!

    Tom.

    Reply
  • avatar
    November 8, 2016 at 12:08 am
    Permalink

    Hi Zoe–

    Per our twitter exchanges (I’m @DaveKeto), my N=1 research to date includes 32 NMRs where I identify a very distinctive *inverse* relationship between dietary fat and corresponding LDL cholesterol (-C, -P, and Small -P). I further recruited my sister (who has a very different lipid profile) for the Identical Diet experiment where we ate exactly the same food (including weight) for 13 days and took 7 NMRs which likewise show matching inversions and tight pattern correlations with each other’s numbers (http://cholesterolcode.com/cholesterol-code-part-v-more-fat-less-cholesterol-to-the-second-power/).

    In the most recent experiment I induced a record drop in my cholesterol over 3 days in the first public presentation of my data with LDL-C dropping by 73 and LDL-P dropping by 1115! (http://cholesterolcode.com/cholesterol-code-part-v-more-fat-less-cholesterol-to-the-second-power/)

    I bring this to your attention with regard to FH in particular. The lipid system is FAR more agile and responsive than modern medicine believes it to be. My own data is putting to rest the clearance presumption as showing much stronger evidence that the body is in fact up and down regulating lipids based on incoming energy (and mostly likely dietary fat). This is particularly relevant to FH as it is a foundation for the argument that high cholesterol is atherogenic.

    Their theory: FH mutated LDLr => lower binding to LDLp Apos => higher cholesterol remaining in the blood — Low “clearance” leading to metabolic “backing up” of serum cholesterol.

    But what everyone seems to be missing is that there’s a particularly GOOD reason for a system with FH to ***upregulate*** LDLp.

    If you, Zoe (who doesn’t buy into the diet-heart hypothesis like so many of us) knew you had FH and thus your cells had poor reception to LDL particles that your cells desperately need for energy, nutrition, and repair — you’d want to *stimulate* LDLp production! Why have 500 LDLp when you could have 1000? 2000? Whatever it took to ensure proper saturation of these vital elements needed throughout your body. Give those poor LDLrs more opportunities to bind by providing more targets.

    Remember bobbing for apples? If those apples were the only way your kid would eat and having a few in the barrel was just too hard for her compared to others, you’d go ahead and fill the bucket until it was easy.

    People dying more often of CVD with FH doesn’t surprise me given the LDLr is a critical pathway to proper cell nourishment and thus I’d assume there’s more endothelial damage/dysfunction under such circumstances. But for goodness sake, if this does turn out to be true, adding a statin is one of the very last things I’d ever do.

    Reply
    • avatar
      November 8, 2016 at 8:15 am
      Permalink

      Hi Dave – lovely to e-meet you! Looks like we came to the same conclusion – FH needs something to stimulate LDL production!

      I’m following you now – keep experimenting! This is one to bear in mind – the complete inaccuracy of the whole shooting match anyway http://www.bmj.com/content/298/6689/1659

      Best wishes – Zoe

      Reply
    • avatar
      November 9, 2016 at 2:22 pm
      Permalink

      I recently had my LDLp counted: 3,500. It was highlighted as too high. Should I be worried or is it a good thing after all?
      LDL particle size: large buoyant only, no small dense.
      Total cholesterol: 11.25
      HDL is fine, triglycerides low, LDL 8.25

      I was told in 1991 that I had FH. I was 24 and put on statins, which I took for 8 years, then decided to stop. Every since then, I have had to defend my decision to doctors. A gene test has now revealed that I do not have FH.

      Reply
  • avatar
    November 7, 2016 at 11:15 am
    Permalink

    Zoe,

    Starting the programme today with a great deal of optimism that four years of health problems’ symptoms’ treatment may come to an end by treating diet as the root cause. We’ll see what happens – I am optimistic because it all makes sense.

    One thought about the 3,500 in = 3,500 out debate: it may actually not be as wrong as you believe. Let me explain my thinking. We now know a lot more about the microbiome and are beginning to realise that what goes into the mouth does not necessarily enter the body (as well as learning that what sometimes enters the body through the gut really shouldn’t – my problem I think is inflammation). So 3500 calories into the body may well need to equal 3500 calories out to lose weight but 3500 calories in the mouth doesn’t necessarily equal 3500 into the body.

    If my thinking is not too far from the mark, it will equal a seriously wide variance depending on individual microbiota make-up. Far from an expert in this so very interested in your thoughts.

    Reply

Leave a Reply

Your email address will not be published. Required fields are marked *