According to advocates of low carbohydrate diets a key benefit is the effect on triglycerides in the blood. The argument goes that a high level of triglycerides is linked to increased risk for coronary heart disease; low carb diets lower triglycerides; so low carb diets should lower the risk for heart disease. Sounds plausible enough, but is it true?
Blood lipids and heart disease risk
The approach to managing blood lipids to lower heart disease risk has evolved over time as our understanding of this complicated field has grown. Decades ago the focus was on lowering total cholesterol but this was later narrowed down to LDL-cholesterol – ‘bad’ cholesterol for the lay person. ‘Good’ HDL-cholesterol was considered protective and the balance between the bad and the good – the LDL/HDL ratio – came into use. More recently, the total cholesterol/HDL ratio has been considered to be a better measure as all non-HDL-cholesterol appears to increase heart disease risk.
What about triglycerides?
If you are interested in how triglycerides affect the risk for heart disease and how diet affects blood triglycerides look no further than the American Heart Association’s scientific statement Triglycerides and Cardiovascular Disease. You may need to allocate an afternoon as the paper is very comprehensive and has over 500 references.
The AHA report states that high levels of triglycerides are associated with higher risk for heart disease but then delves into the long-standing debate about whether high triglycerides actually promotes heart disease or is simply a marker of risk.
The issue here is that high triglycerides are often associated with low levels of protective HDL-cholesterol. In fact, the two are metabolically linked – if triglycerides go up, HDL-cholesterol goes down. As low levels of HDL-cholesterol strongly predict higher heart disease risk, HDL seems to be the key player and triglycerides its faithful companion.
Image: source
Factors affecting triglycerides and HDL
Several aspects of diet and lifestyle affect triglycerides and HDL-cholesterol in the blood. Weight loss of 5-10% results in a 20% fall in triglycerides and increases HDL-cholesterol. Similar effects can be achieved with increased physical activity. Long chain omega 3s or fish oils also lower triglycerides, though quite high intakes are required to achieve the effect. And high intakes of alcohol can increase triglycerides. The amounts of fat and carbohydrate in the diet are relevant too.
High carbohydrate diets: adverse effects?
Very high carbohydrate diets certainly raise triglycerides and lower HDL-cholesterol. This is one of the reasons that the US Institute of Medicine and the NHMRC recommend upper limits of carbohydrate intake of 60-65% of calories. If these upper limits appear high it’s because increasing the carbohydrate content of the diet at the expense of saturated fat also lowers total and LDL-cholesterol – beneficial effects.
So when considering the effects of high and low carbohydrate diets it’s important to consider overall effects on blood lipids. Just focussing on triglycerides will only tell part of the story.
Carbohydrate quality
Carbohydrate-rich foods vary enormously – from jelly beans to red kidney beans – and it would not be surprising to find that different carbohydrate-rich foods affect blood lipids differently. The DASH diet was rich in carbohydrate from fruits, vegetables and wholegrains and lowered blood pressure, but it did not raise triglycerides. Carbohydrate quality was high and consequently high carbohydrate intake did not adversely affect blood lipids.
Fructose has a reputation for being triglyceride-raising though a meta-analysis showed that replacing starch or sucrose with fructose had no effect on fasting triglycerides at intakes of up to 100g a day. The triglyceride-raising effect was observed at higher intakes of fructose. Another meta-analysis suggested that people with diabetes, who are prone to high triglycerides and low HDL, may be more sensitive to fructose. But intakes of over 60g a day were still needed to demonstrate an effect on triglycerides, which equates to about 12% of calories in a 2000 calorie diet. So even in this at-risk group the fructose message is about moderation rather than avoidance.
New meta-analysis: sugars and blood lipids
A new meta-analysis of studies into the effect of sugars on blood lipids was published by Te Morenga and colleagues in May of this year. As expected they reported that higher sugar intakes are associated with higher blood triglycerides but perplexingly they found that sugars raised the level of protective HDL-cholesterol. This doesn’t make much sense given the metabolic link between the two. One of the problems with this study is that it is not clear what sugars are being compared to. Is it starch, or total fat, or specific types of fat?
Sugars were found to increase LDL-cholesterol but again we don’t know what the reference is. Based on previous work it could be expected that sugars would raise LDL-cholesterol compared to polyunsaturated fat but lower it relative to saturated fat. The reference is critical to the finding. Unfortunately, effects on overall measures of lipid-related risk, such as the total cholesterol/HDL ratio, were not reported. And some of the studies included did not have strict control of energy intake, which is interesting given the effects of positive and negative energy balance on blood lipids. Quite a few of the studies were conducted in the 1960s or 70s and heterogeneity was high.
Make up your own mind on this one. It’s clear that we need some new, well designed studies to guide policy on sugars.
Image: source
Low carbohydrate diets: good or bad for blood lipids?
The effect of carbohydrate on triglycerides is a weak rationale for recommending a high or low carbohydrate diet. Overall effects on blood lipids need to be considered and in the case of low carbohydrate diets this will largely be determined by the type of fat that replaces carbohydrate. If it is unsaturated fat, as recently trialled by CSIRO in people with diabetes, a low carbohydrate diet confers benefit. However, there is no benefit if saturated fat is used to replace carbohydrate.
One of the lingering mysteries about the current enthusiasm for low carbohydrate diets is the frequent recommendation by unqualified, self-declared authorities to increase intake of saturated fat, rather than unsaturated fats.
Hmmm. Why would anyone make such a recommendation?
Well done with this one Bill. takes me back to 1970 when I worked with Joan Woodhill in the lipid lab at Prince Henry Hospital Sydney (Little Bay). One anecdote, a patient encouraged to stop smoking, took up Minties, ended up with heart disease and elevated blood sugars, triglyceride/cholesterol.
Hi Bill. As that smoker was already in your lipid clinic I suspect that the heart disease was well and truly underway pre-Minties. But to get ourselves on TV I think we should ignore all that risk factor stuff and mount a high profile campaign to ban Minties Australia-wide. We can claim cause and effect – the guy ate Minties and he got heart disease. Bill, that’s not evidence; it’s proof!
I am going to live on a farm. Regards, Bill
See I’ve done lots of study and I’m not agreeing with you Bill! I’ve concluded that I need plenty of saturated fat to maintain my hormones and cell membranes and brain health. I don’t take this lightly I had a grandmother die of a heart attack in her mid-forties and a grandfather on the other side have a heart event and subsequent bypass operations on the other side and my Dad had a stroke. Let me show you a few of the studies that convinced me, I’m sure you have read them, tell me how I am misinterpreting them please! http://www.ncbi.nlm.nih.gov/pubmed/20071648?dopt=AbstractPlus and http://www.ncbi.nlm.nih.gov/pubmed/20089734?dopt=AbstractPlus and http://www.ncbi.nlm.nih.gov/pubmed/20685950?dopt=AbstractPlus and http://www.ncbi.nlm.nih.gov/pubmed/15531663?dopt=AbstractPlus.
Jenny, saturated fat is not an essential nutrient. Your body can make it. Regards, Bill
Two words Bill: breast milk! Full of sat fat and cholesterol!! Crisis!!! Stop the breast feeding now! My degree (one of them) is in zoology (mammal evolution emphasis) and I also did human biochem and physiology! And I am astonished that you are sticking to your PUFA guns, astonished! I have been asking the question for decades now, how can saturated fats be bad when we are full of them and animals are full of them and they are so stable? I’ve got my answer: they are not bad!
Did you not read what Bill said? SFA is not an essential fat, we can make it. Do you think cows are eating a ton of saturated fat? No, free-range cows eat a plant-based diet- grass!
Thanks Emma. Would you like the list of essential nutrients that we can’t make ourselves that are found in animals products and whose uptake is assisted by saturated fat: choline, vitamin K2, vitamin D and vitamin A.
Hi Jenny. The absorption of fat-soluble nutrients is facilitated by any sort of fat. Saturated fat is not required for their absorption. Regards, Bill
Emma cows are ruminants and herbivores, they have 4 stomachs. They are not like us!
Vitamine D ???? We can of course make it ourself with only 20 min exposure to sun.
The fatty acid content of breastmilk varies according to the mother’s diet. If she is in energy balance up to 85% of fatty acids will come from her diet. There will certainly be some saturated fat as a result of synthesis in the breast tissue and mobilisation of fat stores if required but breastmilk doesn’t contain just saturated fat and depending on the mother’s diet saturated fat won’t be the dominant fatty acid.
Ok.
Abstract from the first study
” More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.”
- Studies since then have shown benefits of replacing saturated fat with polyunsaturated. Also – PREDIMED study has shown clear benefits from a diet high in olive oil
The second one.
“In summary, although substitution of dietary polyunsaturated fat for saturated fat has been shown to lower CVD risk, there are few epidemiologic or clinical trial data to support a benefit of replacing saturated fat with carbohydrate. ”
The third one.
- No mention of poly/mono fats in the abstract
The 4th one
- comparing with carbohydrate – not poly/mono fats.
None of those studies can justify using saturated fat in favour of poly/mono fats. A diet high in refined carbohydrates in not a healthy diet – wide agreement on that point.
Thanks Paul. Interesting thoughts. I wish I could get past the chemical instability of those seed oils! http://www.ncbi.nlm.nih.gov/pubmed/25264922
And the dangers to your health! http://www.ncbi.nlm.nih.gov/pubmed/23386268
I really wish you would stop peddling those dangerous seed oils!
Jenny,
You don’t need to get past the ‘chemical instability” of seed oils to replace saturated fat with mono/poly fats.
Use olive oil!!!! And eat nuts!!!! This is what I advocate. Whoever said I was ‘peddling those dangerous seed oils’?????
I noticed you link was to the re-analysis of the Sydney diet heart study. This study used a high trans fat margarine, which is no longer available in Australia. Margarines in Australia in 2014 are nearly all less than 1% trans fat. So this study is of highly questionable relevance to the Australian market in 2014. I would like to see a study like this repeated with the products we have available today, as that would give a clearer answer to the question.
I would suggest looking up the ‘PREDIMED’ study which used olive oil, and used nuts.
Everyone is in agreement that products high in trans fat should be avoided.
Exactly- I get my fats from nuts, seeds, olive oil, oily fish and avocado and reduce my consumption of others (including dairy fats and processed fats). So easy, so delicious, and we surely we can all agree those food fat sources are nutritious. Mediterranean style diet ticks every box for me..The real problem is the fact that the price of the nuts/seeds/oily/fish/avocado are far more expensive than ‘dangerous seed oils’ and other processed foods. Thats where population health needs to focus its efforts and arguments on…
Hi Paul, I was not seeing you as a ‘peddler of seed oils’ I was really thinking of Bill! And yes I use an abundance of olive oil and macadamia oil as well as butter and avocado and coconut oil. I have to be pretty careful with nuts generally as I am allergic to walnuts. I try to research the processes used to produce the oils because I am concerned about toxins. I continue to be very concerned about the arachidonic acid–derived eicosanoids that tend to form from excessive Omega -6 consumption which drive many of the inflammatory diseases so prevalent today. And sorry when I was referring to the “chemical instability” of the unsaturated oils I was referring to the actual chemical nature of the compound, PUFAs being orders of magnitude more reactive than MUFAs and SaFA. Sorry to get too technical for you.
I followed the link to the responses on the Sydney Heart Study. The author, Chris Ramsden, made some defense against Paul’s point about trans fat. Some of it seems weak, but he did point out that the intervention group had lower LDL which would go against the expected effect of trans fat. Really, though the study had 16 deaths in one arm and 10 deaths in the other so any number of things could have easily biased the results. The author seems to be more interested in promoting a hypothesis about oxidized linoleic acid causing the outcome. But interestingly Ramsden does not agree with much last statement either, Jenny. He says elsewhere that increased linoleic acid in the diet doesn’t increase arachidonic acid leading to inflammation (and pretty much everything else I’ve read on the subject except Wikipedia). https://evolvinghealth.wordpress.com/2013/04/23/does-linoleic-acid-lead-to-inflammation-and-cardiovascular-disease/#more-788
Hi Joe, yes! Lots to think about. It does depend on how deep you dig!
Joe, remember that the changes were replacing saturated fat + trans fat with polyunsaturated fat + trans fat. Hence, it is unlikely that there were major differences between the groups in trans-fat intake as Ramsden et al. had explained – http://www.bmj.com/content/346/bmj.e8707/rr/631590
Also watch out for the double-standard here. Those who dismiss the SDHS based on possible confounding usually accept other studies where confounding was known (bias against saturated fat groups), such as the ODHS and STARS. They would even accept studies that used inappropriate designs such as the FMHS.
Everyone is in agreement NOW to avoid trans fats, but the reason everyone ate trans fats in the first place is that they were told saturated fat was bad for them!
Also, there is no such food as a pure saturated fat. Butter fat is about 40% MUFA. If you eat more fat, you eat more PUFA, even without seeking out seed oils.
Coconut oil is about 80% saturated fat
I have a MSc(Hons) Organic Chemistry, spent years working on drug interactions and pharmacy IT computer programs. Now retired, with a wife with MS. A friend suggested the keto diet, so I checked out various sources, and my wife started the low carb diet late October. I am acting as the “control” – my diet is 100-150gms/day, hers is 30-50gms/day. Prior to this diet (to mid October) my wife was on a strict low saturated fat diet of less than 15gms/day.
I have a spreadsheet and count total calories, Protein, total Fat, (and lately) saturated fat, and carb. We are aiming at a diet high in green leafy vege, avocado, Nuts, Omega 3 rich fish and poultry. I am still having limited cereals and up to one slice of homebaked bread a day. The initial focus was getting my wife to Keto, but I am slowly working to minimise saturated fat, at least the long chain varieties. Short chain saturated fat is healthy – there are no short chain unsaturated fats!)
After one month, we have both lost a similar amounts of weight (6-8kgs). (Initial weight loss is often mostly water) I have always had low BP, but my wife has had serious, uncontrolled high BP, with medicine unable to bring it down much. Over November, her BP has moved from 144/91 to 127/83 (averages). Importantly, no more very high BP readings. Her circulation in her toes has improved. She is not hungry, even though on reduced calories. I am suffering hunger pangs, as I am still moderately high carb.!!! This is why many on low fat, moderate to high carb diets give up, as the hunger pangs are too great.
Negatively, no signs of improvement in her MS, but this could take 2 years. Ketone bodies enter the Krebs cycle in a different way, so that energy is released with fewer free radicals. The theory is that less damage is caused to the Neurons, which are then able to remyelinate – (or at least, slow down the rate of damaging lesions). No signs of improved energy levels (MS is draining!)
I am studying up as I go, trying to improve my understanding of nutrition. My background in chemistry, research and pharmacology helps.
I am a natural skeptic, and don’t “believe” in any nutritional position. Nutrition, particularly lipid metabolism, is in a state of flux, and the drug companies and their statins have money in this game. Money in the low carb? There are many not-for-profits pushing low carbs, along with many pushing their diet books and products.
Dr Peter Attia is a good source of honest opinion. He is “a paid employee of NuSI, a California-based 501(c)(3) which funds independent researchers who investigate the relationships between diet and the metabolic diseases associated with obesity”
Nutrition is going through a massive paradigm shift from High Fat bad to high fat good. As in all areas where science claims a false “consensus” (such as human caused global warming when the Earth is actually cooling – yes, I said I was a skeptic)!!
The truth is that we have had very poor Nutrition science over the last 50 years or so, and the health of the West had badly suffered with Obesity and diabetes on the rise.
Interesting times.
Hi Ross.
Science teaches us to be sceptical.
You say we have had very poor nutrition science over the last 50 years or so – a comment frequently heard. However, I think it needs a little context. Once nutrition science worked out all the requirements for essential nutrients a new phase of nutrition science began. This focussed on the role of nutrition in reducing the risk for chronic diseases, such as cardiovascular disease, cancer, diabetes and obesity. The first Dietary Guidelines for Australians were published about 35 years ago and summarised the nutrition science available at the time. By today’s standards you could say this science was relatively poor, but it was the best available at the time. It was a whole new field.
ONE of the recommendations was to ‘eat less fat’- good catch-all advice that it was thought would lower the risk for several chronic diseases. But then nutrition scientists undertook some very large, very good studies to test the hypothesis.
Very unfortunately, despite the quality of the science, many nutritionists refused to believe the results: ‘Eat less fat’ was NOT evidence-based advice – it did nothing. We knew this in 2006. Health authorities should have adjusted their advice much earlier but the wheels turned very slowly and the conservatism ran deep. We are paying the price for it now. Nutrition authorities are being beaten over the head by lay ‘experts’ purporting to have discovered that low fat diets don’t work. They didn’t do the research!
Nutrition science now needs to reassert itself and reclaim its authority. Regards, Bill
Low carb proponents are generally of the opinion that a) saturated fat is not a bad thing per se, b) increased dietary saturated fat does not correlate with increased saturated fat in the blood stream and c) if you take out carbohydrates you need a replacement energy source and given a) and b) why not use saturated fat if you wish to avoid inflammatory seed oils.
There is also evidence that in low carbohydrate diets the saturated fat is preferentially oxidised as fuel so it generally isn’t seen as an issue. Reams of weak epidemiology about sat fat in the context of a high carbohydrate intake isn’t going to sway anyone on this I suspect.
Bill,
I am a 28 year old male with very normal blood pressure, blood sugar and blood lipid levels. I limit my calories and alcohol and I do a mix of cardio and strength exercise.
Since I don’t seem to be at risk for chronic illness like heart disease or diabetes, how can a guy like me incorporate so-called “poor carbohydrates” into a healthy diet? I am a big believer that any diet should be enjoyable to the individual to be sustainable over the long term. I eat jasmine rice and pasta and potatoes and bread and coconut milk because I enjoy them and I can factor other very nutritious foods around them.
What is some sound, workable and simplistic advice I can follow to enjoy eating these foods without stressing myself out too much in the process?
Hi Derick
I totally agree with you that a healthy diet should be both enjoyable and sustainable. Extreme or purist approaches usually fail on both counts.
Regarding ‘poor carbohydrates’, the definition is still not universally agreed. But if we define it as nutrient-poor carbohydrate-rich foods that have a high GI and/or lacking in fibre we are looking at foods like white rice, baked goods (biscuits, cakes, pastries), confectionery and many sugar-sweetened beverages. Many of these are treat foods which contribute to enjoyment but don’t do much for nutrition.
So, for a young, healthy person such as yourself, the answer is ‘moderation’.
Personally, I don’t quantify how much of these foods I eat. Rather, I respond to the circumstances, so intake varies from day to day. Maybe I should write a book ‘The Commonsense Diet’.
Regards, Bill
Bill, I would appreciate your response to this recent meta- analysis (link below)
Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysi
http://openheart.bmj.com/content/2/1/e000196.full
thank you
Hello Elmarie. When it comes to the question of whether the evidence available in ~1980 justified the introduction of a dietary guideline on fat, my answer is yes and no.
The randomised controlled trial evidence, which the latest meta-analysis addresses, was mixed. Other meta-analyses have different findings, so I guess we can still say the evidence is mixed.
But when those first dietary guidelines were put together the scientists didn’t just look at RCTs. They also looked at data from animal studies, epidemiological evidence, and mechanistic studies – especially the effects of different types of fat on blood cholesterol. In the end, it was decided that the evidence supported the replacement of saturated fat with polyunsaturated fat. But how would this be communicated to the general public?
THIS was where the big mistake was made. It was assumed that the average person wouldn’t be able to understand ‘replace saturated fat with polyunsaturated fat’ or even ‘lower saturated fat’. So, it was decided that the simple message would be ‘eat less fat’. If people followed it, saturated fat intake would go down as total fat intake went down (and carbohydrate intake went up).
People weren’t concerned that there might be a negative side effect to ‘eat less fat’. In fact, it was thought that ‘eat less fat’ might lower the risk for breast cancer, bowel cancer and overweight.
Thirty years later we worked out that the original message – replace saturated fat with polyunsaturated fat – was actually the correct one and that ‘eat less fat’ (which encouraged people to replace all type of fat with carbohydrate) achieved nothing.
‘Replace saturated fat with polyunsaturated fat’ is what we should be implementing now but lots of people are muddying the waters for one reason or another. Regards, Bill