Consumption of Dairy Fat Doesn’t Increase the Risk of CVD — may protect

A new study published this week in the American Journal of Clinical Nutrition reports that long-term consumption of the saturated fat found in full-fat dairy products is not associated with an increased risk of cardiovascular disease (atherosclerosis, coronary artery disease, etc.) or other causes of death, and may actually be protective against heart attack and stroke[1].

The study which took place over almost a quarter of a century measured three specific fatty acids found in dairy products in 2,900 older adults, aged 65 years and above— first in 1992, again in 1998 and finally in 2015. The three fatty acids they measured were pentadecanoic, heptadecanoic, and palmitoleic acids.

During the 22 year period, 2,428 of the participants died of which 833 were due to heart disease.  When the data was analyzed, none of the three fats was associated with the risk of total mortality (death) or heart disease — in fact, high levels of heptadecanoic acid was associated with a lower risk of death from heart disease and stroke.

This is significant because while higher amounts of saturated-fat consumption, including the saturated fats in this study increase blood LDL cholesterol, they also increase HDL cholesterol and decrease triglycerides[2], both of which are protective. Since it was unknown what the ‘net effect’ on total mortality (death) and cause-specific death, this study was done to determine what effect, if any increased dairy fats had on these outcomes.

The results were clear.

Not only did long-term consumption of these three dairy fats have no effect on either total death or heart disease, high levels of one of the fats found in full-fat dairy was actually found to be associated with a lower risk of heart disease and stroke!

The authors of the study conclude;

“For decades dairy fat consumption has been hypothesized to be a risk factor for CVD, as well as potentially diabetes, weight gain, and cancer, little empirical evidence for these effects existed from studies of clinical events. In current years, a growing number of prospective studies have shown generally neutral or protective associations between self-reported dairy foods and dairy fat consumption with the risk of CVD, diabetes, weight gain and cancers, raising questions about this conventional wisdom.”

The results of this long-term study with almost 3,000 older adults demonstrates that the saturated fat found in full-fat dairy is not associated with cardiovascular disease (CVD), diabetes or cancer and may even be protective against both heart attack and stroke.

Final Thoughts…

With both the American and Canadian Dietary Guidelines currently being revised— and “front of label labeling” in Canada to advise against foods high in saturated fat, it is time for both the US Office of Disease Prevention as well as Health Canada to review their respective recommendations with regards to consumption of low-fat dairy, in light of current research.

Dairy protects play an important role in health and nutrition and are rich sources of calcium, potassium, and phosphorus and are a ready supply protein and essential fat not only to growing children, but to older adults who risk osteoporosis and sarcopenia (muscle wasting). Given the results of this study on the saturated fat in dairy, as well as the results of a recent 158-country study which found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease, it is time to  re-evaluate the long-held belief that animal fat (whether in meat or dairy), is somehow ‘dangerous’.

A Few Words “Fat Phobia”

I regularly come across people in my practice who grew up in the last 40 years and who have spent their entire lives avoiding any form of animal fat.  The very idea of eating the yolk in egg is a source of anxiety — and it need not be so.

I am not suggesting that these folks suddenly start eating copious amounts eggs, meat, cheese, cream and butter but often suggest they start with things such as avocado, olives, nuts and seeds that are rich in monounsaturated fats that have been less villainized than saturated fat. I encourage them to use a little cream on top of fresh berries or use a bit of butter to cook with. In time, I may show them delightful egg recipes that have other foods they are used to eating and enjoy, such as a spinach-ricotta pie, which makes a lovely summer-time dinner when it’s too hot too cook.

Overcoming “fat phobia” takes time — especially when it has been ingrained in you since you’re young. I understand. When we work together, you set the pace.

People are sometimes concerned than they can’t follow a low-carbohydrate lifestyle because they “can’t eat all that fat”, but the truth is, not all low-carb diets have large amounts of fat. It’s only because fat has 2  1/2 times the calories as protein and carbs that some types of low-carb diet are still considered “high fat”. There is a whole range of low-carb diets which you can read about here as well as different types of ketogenic (“keto”) diets that you can read about here.

Have questions about which type of low carbohydrate diet may be best for you? Or perhaps you have questions about my services and their costs.  Maybe you’d just like to meet me for a one-hour consultation (in-person or via Skype) to ask questions and see if this may be an option for you. Please send me a note using the “Contact Me” form on this web page and I’ll be glad to reply as soon as I’m able.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


 

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Otto MC , Lemaitre, RN, Song, X et al; Serial measures of circulating biomarkers of dairy fat and total and cause-specific mortality in older adults: the Cardiovascular Health Study,The American Journal of Clinical Nutrition, https://doi.org/10.1093/ajcn/nqy117
  2. Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr 2003;77(5):1146–55

 

CVD Risk Improves By Use of Ketogenic Diet in Type 2 Diabetes at 1 year

One of the concerns raised by opponents of a very low carb or ketogenic diet is that it increases risk of cardiovascular disease such as heart attack and stroke, but does it?

Results of a peer-reviewed study of cardiovascular outcomes of people with Type 2 Diabetes (T2D) that was published at the beginning of May in the Journal of Cardiovascular Diabetology[1] found that those that followed a ketogenic diet significantly improved in 22 of 26 cardiovascular disease risk factors, including biomarkers of cholesterol / lipoproteins, blood pressure, inflammation, and carotid intima media thickness (cIMT).

Previous published results from the same researchers and published in February of 2018 demonstrated that reversal of T2D symptoms was able to be achieved and sustained long term using a ketogenic diet[2,3].

Simply by decreasing the amount of carbohydrate in the diet over the course of a year there was not only a significant decrease in blood sugar and weight, but a dramatic improvement in lipid and lipoprotein markers associated with markers of cardiovascular risk.

The results of this most recent study do much to dispel the myth that a therapeutic ketogenic diet puts individuals at increased risk for heart attack and stroke. In fact, it reduces their risk.

Methods

Continuous Care Intervention (CCI) Group Participants

At the beginning of the study, there were 238 participants enrolled in the continuous care intervention (CCI) group and all had a diagnosis of Type 2 Diabetes (T2D) with an average HbA1c of  7.6%  ±1.5%.  They ranged in age from 46 – 62 years of age, 67% were women and 33% were men. Weight of the subjects ranged from 200 pounds to 314 pounds (117±26 kg) with an average weight of 257 pounds (117 kg) and Average Body Mass Index (BMI) was 41 kg·m-2 (class III obesity) ±9 kg·m-2, with 82% categorized as obese.  The majority of participants (87%) were taking at least 1 medication for glycemic control medication.

At the end of a year, 218 participants (83%) remained enrolled in the  continuous care intervention (CCI) group.

Intervention and Monitoring of CCI Group

Each participant in the CCI group received an Individualized Meal Plan which enabled them to attain and maintain nutritional ketosis. They also received behavioral and social support, biomarker tracking tools, and ongoing care from a health coach with medication management by a physician.

Subjects typically required <30 g·day−1 total dietary carbohydrates.

Daily protein intake was targeted to a level of 1.5 g·kg−1 based on ideal body weight and participants were coached to incorporate dietary fats until they were no longer hungry.

Other aspects of the diet were individually tailored to ensure safety, effectiveness and satisfaction, including consumption of 3-5 servings of non-starchy vegetables and sufficient mineral and fluid intake.

Participants ability to achieve and maintain nutritional ketosis was determined by subjects monitoring their blood ketone level of β-hydroxybutyrate (BHB) using a portable, handheld device. Blood glucose and β-hydroxybutyrate (BHB) levels were initially tracked daily using a combination blood glucose and ketone meter and frequency of tracking was modified by the care team based based on each individual’s needs and preferences.

Participants with high blood pressure (hypertension) were provided with an automatic home blood pressure machine (sphygmomanometer) and they were instructed to record their readings daily to weekly in the supplied app, depending on recent blood pressure control. Antihypertensive medication prescriptions were adjusted based on home blood pressure readings and reported symptoms.

Downward Adjustment and/or Discontinuation of Medications

As blood pressure came down, diuretic medication was the first antihypertensive medication to be discontinued. This was followed by beta blockers (unless the participant had a history of coronary artery disease).

Angiotensin-converting-enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) were generally continued due to their known protective effect on the kidneys in those with Type 2 Diabetes.

Statin medications were adjusted to maintain a goal of LDL-P under 1000 nmol L−1 (or based on participant preference after full risk/benefit discussion with the physician).

The Usual Care (UC) Group

For comparison purposes, an independent group of patients with Type 2 Diabetes were also recruited for the study and were referred to Registered Dietitians that provided dietary advice according to the American Diabetes Association Guidelines [4].

Laboratory Assessors

Since an abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) is a known risk factor for CVD [5] and is very common in people with Type 2 Diabetes, a number of laboratory tests were conducted at the beginning of the study and the end to determine if they improved, stayed the same or got worse.

Most common in people with Type 2 Diabetes is where there are increased triglycerides (TG), decreased high-density lipoprotein cholesterol concentration (HDL-C) and increased small low-density lipoprotein particle number (small LDL-P).

The authors of this study state that evidence suggests that increased very low-density lipoprotein particle number (VLDL-P) and a large VLDL-P in particular may be one of the key underlying abnormalities in this abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) associated with T2D.

The authors also outline how higher concentrations of small LDL are often associated with increased total LDL particle number (LDL-P) and increased ApoB which is the main protein constituent of  very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL). The authors provide previous study evidence that demonstrates that in people with insulin resistance and T2D, increased total LDL particle number (LDL-P) and increased ApoB may exist even with normal to low LDL-C concentrations values. For this reason, LDL-C alone was not relied on as a measure of abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) in this study as it could miss the impact of increased total LDL particle number (LDL-P) and/or ApoB.

The authors mentioned that in previous studies with carbohydrate restriction of up to 1 year, while triglycerides (TG) usually decrease and HDL-C often increase, LDL-C sometimes increased and other times decreases. The authors note that although higher LDL-C is a known risk factor for CVD, low LDL-C may also reflect higher small, dense LDL, total LDL particle number (LDL-P) or ApoB and thus be a risk factor, as well.

Since inflammation is involved at all stages of the atherosclerotic process, higher high-sensitivity C-reactive protein (CRP) and/or higher white blood cell count (WBC) were assessed as risk factors for CVD.

Finally, since high blood pressure (hypertension) is also an added risk factor for CVD in people with T2D, tighter blood pressure control was deemed to reduce the risk of DVD, stroke and other microvascular events.

Continuous Care Intervention (CCI) Group

Standard laboratory fasting blood draws of the CCI group were obtained at the start of the study (baseline), at 70 days (3 months) and at ~ 1 year follow-up.

Lipid/cholesterol-related tests included ApoB, ApoA1, total cholesterol, triglycerides, direct HDL-C concentrations and LDL was calculated using the Friedewald equation.

The LipoProfile3 algorithm was used to determine relationship of lipid subfractions to cardiovascular (CVD) risk – specifically the number of HDL particles (HDL-P) previously reported  to be associated with death, Myocardial Infarction (MI), stroke and hospitalization, HDL-C (HDL cholesterol) which is the amount of cholesterol those particles are carying, which is not associated with these negative outcomes and HDL-P subclasses [6].

Risk was also determined using the lipoprotein insulin resistance score (LP-IR) which was proposed to be associated with the homeostasis model assessment of insulin resistance (HOMA-IR) and glucose disposal rate (GDR) [7].

Finally, risk was also determined using the 10-year atherosclerotic  cardiovascular disease (ACSVD) risk score of the American College of Cardiology [8].

Carotid ultrasonography (cIMT) measure was performed at baseline and 1 year to characterize atherosclerotic risk.

The Usual Care (UC) Group

Body measurements, vital signs and fasting blood draws for the Usual Care (UC) group were obtained at the start of the study (baseline) and at 1 year using the same clinical facilities and laboratory and data collection methods. Carotid ultrasonography (cIMT) measure was also performed at baseline and 1 year to characterize atherosclerotic risk.

Results

There were no significant difference in the baseline characteristics of the two sub groups of CCI participants (web-based on onsite-based) and no significant difference at 1 year, so for the purpose of analysis, data from both groups were combined.

As well, there were no significant difference in the baseline characteristics of the Usual Care (UC) group (which served as an observational comparison group) and the Continuous Care Intervention Group (CCI) except mean body weight and BMI were higher in the CCI versus the UC group.

The within-Continuous Care Intervention group changes in the following lipids and lipoproteins were all statistically significant and were as follows; ApoA1  [a component of high-density lipoprotein (HDL)] increase by + 9.8%) ApoB / ApoA1 ratio decreased by − 9.5% Triglycerides (TG) decreased by − 24.4% LDL-C increased by + 9.9% but LDL-particle size also increased by + 1.1% (that is, large fluffy LDL increased compared with small, dense LDL) HDL-C increased by + 18.1% total HDL-P increased by + 4.9% large HDL-P increased by 23.5% Triglyceride/ HDL-C ratio decreased by − 29.1% large VLDL-P decreased by − 38.9% small LDL-P decreased by − 20.8% There were no significant changes in total LDL-P or ApoB.

These results are impressive!

Simply by decreasing the amount of carbohydrate in the diet over the course of a year there was a dramatic improvement in lipid and lipoprotein markers associated with markers of cardiovascular risk.

In addition, the Continuous Care Intervention group had a significant reduction in;

systolic blood pressure decreased − 4.8%

diastolic blood pressure decreased − 4.3%

C-Reactive Protein (CRP) decreased almost 40% (i.e. − 39.3%) 

white blood cell (WBC) count decreased − 9.1%

Below are graphs of the changes in biomarkers for the Continuous Care Intervention (CCI) group (figure 1) and the Usual Care (UC) Group;

FIGURE 1: changes in biomarkers for the Continuous Care Intervention (CCI) group

 

FIGURE 2: changes in biomarkers for the Usual Care (UC) group

Below is a comparative graph of the two groups, the Continuous Care Intervention (CCI) Group and the Usual Care (UG) Group

FIGURE 3: changes in biomarkers for the Continuous Care Intervention (CCI) group compared to the Usual Care (UC) group

Some Final Thoughts…

This study demonstrates that a therapeutic ketogenic diet followed over the course of 1 year significantly improved 22 of 26 cardiovascular disease risk markers in those with Type 2 Diabetes. This is huge!

The size of the study group was large and had an 83% retention rate over the course of the year – which in and by itself demonstrates that the intervention diet was one that people had no difficulty staying with in their day-to-day lives, without the use of meal replacements (shakes or bars).

While not a randomized control trial between CCI and UG groups, this study supports that a ketogenic diet is both safe and effective for periods of up to a year (and in other studies has been documented to be safe and effective for up to two-years). Not only can a well-designed ketogenic diet reverse many of the symptoms of Diabetes (documented in this earlier article) it can also significantly improve risk markers for cardiovascular disease.

Do you have questions about how a carefully-designed low carbohydrate or ketogenic diet can help you improve symptoms of Type 2 Diabetes and lower markers of risk factors for cardiovascular disease?

Please send me a note using the “Contact Me” form above to find out more about how I can provide you with in-person or Distance Consultation services (via Skype or long distance telephone).

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Bhanpuri NH, Hallberg SJ, Williams PT et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)
  2. McKenzie AL, Hallberg SJ, Creighton BC, Volk BM, Link TM, Abner MK, Glon RM, McCarter JP, Volek JS, Phinney SD, A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes, JMIR Diabetes 2017;2(1):e5, URL: http://diabetes.jmir.org/2017/1/e5, DOI: 10.2196/diabetes.6981
  3. Hallberg SJ, McKenzie AL, Williams, PT et al. Diabetes Ther (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.
  4. America Diabetes Association, Lifestyle management. Diabetes Care. 2017;40 (Suppl 1):S33–S43
  5. Fruchart J-C, Sacks F, Hermans MP, Assmann G, Brown WV, Ceska R, et al. The Residual Risk Reduction Initiative: a call to action to reduce residual vascular risk in patients with dyslipidemia. Am J Cardiol. 2008;102:1K–34K.
  6. May HT,  Anderson JL, Winegar DA, Utility of high density lipoprotein particle concentration in predicting future major adverse cardiovascular events among patients undergoing angiography, Clinical Biochemistry, 2016;49(15): 1122-1126
  7. Shalaurova I, Connelly MA, Garvey WT, Otvos JD. Lipoprotein insulin resistance index: a lipoprotein particle-derived measure of insulin resistance. Metabol Syndr Relat Disord. 2014;12:422–9.
  8. Goff DC, Lloyd-Jones DM, Bennett G, Coady S, D’Agostino RB, Gibbons R, et al. ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;2014:S49–73 (tool: http://tools.acc.org/ASCVD-Risk-Estimator-Plus/#!/calculate/estimate/)

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Two More Good Indicators of Cardiovascular Risk

In a recent article about why Waist Circumference and Waist-to-Height Ratio is so important, I explained that a meta-analysis from 2012 which pooled data from 300,000 adults of different races and ages found that the lowest risk of cardiovascular disease and shorter lifespan was associated with a Waist to Height Ratio (WHtR) of 0.5. That is, we are at lowest risk when our waist circumference is less than half our height (even if our BMI is in the normal range). I also explained exactly how to take waist circumference, so that the results are accurate.

There are other measures of cardiovascular risk that I think are worth considering.

  1. A 2015 study of 3200 adults found that Waist-to-Hip Ratio (WHR) is more accurate in predicting 10-year cardiovascular risk than Waist to Height Ratio (WHtR), however whether this relationship would hold up in a sample as large as the meta-analysis above is unknown. I feel it is worth mentioning Waist-to-Hip Ratio (WHR) as an indicator of cardiovascular risk, as it is easy to do.
  2. Another index this 2015 study found to accurately predict 10-year  cardiovascular risk was something called Conicity Index which I will touch on even though it is not as easily determined as Waist-to-Hip Ratio (WHR) or Waist to Height Ratio (WHtR).

Determining Waist to Hip Ratio

As mentioned in the previous article, to use these indices requires waist measurements and hip measurements to be done accurately and at a specific place on the body.  To make it easier, I will repeat how to measure waist circumference here and below, how to measure hip circumference.

Measuring Waist Circumference

For the purposes of calculating risk associated with increase abdominal girth, waist circumference needs to be measured at the location that is at the midpoint (i.e. half way) between the lowest rib and the top of the hip bone (called the “iliac crest”). Below is a picture that should help.

Where to measure waist circumference

This measurement should be taken with a flexible seamstress-type tape measure, being sure that the tape measure is at the same height in the front and the back, when looking in front of a mirror. That is, the tape measure should be perpendicular to the floor (not higher in the back or the front).

It’s also important that the person’s abdomen (belly) is completely relaxed when taking the measurement, not sucked in.  One way to do that is to taking a deep breath and let it out fully just as the measurement is taken.

If your Waist to Height ratio is greater than 0.5, then you are at increased risk for cardiovascular events and a shortened lifespan. Looking at the graph above, one can see that for every little bit over 0.5, the risk rises steeply.

Measuring Hip Circumference

Hip circumference needs to be measured at the widest portion of the buttocks (butt) and as with waist circumference, the tape measure needs to be parallel to the flood (same height in the front and the back, when looking in front of a mirror).

For both the waist and hip measurement, the tape measure should be snug around the body, but not pulled so tight that it is constricting and it is best if a stretch‐resistant but flexible seamstress-type tape measure is used.

Assessing Waist-to-Hip Ratio

If the waist circumference is measured in inches, then the hip circumference needs to be as well – same if the measurement is in centimeters; both need to be in the same units.

To calculate the Waist-to-Hip Ratio take the waist circumference and divide it by the hip circumference.

Waist-to-Hip Ratio and Risk of Cardiovascular Disease

The following ratios are associated with low, moderate and high risk of cardiovascular risk;

Low Risk: For men, if the ratio is 0.95 or less, for women if the ratio is 0.80 or less

Moderate Risk: For men, if the ratio is 0.96 – 1.0, for women if the ratio is 0.81 – 0.85

High Risk: For men, if the ratio is 1.0 or more, for women if the ratio is 0.85 or more.


The Waist-to-Hip Ratio can also be thought of as people being shaped like “apples” or “pears”.

“Apples” versus “Pears”

People who carry most of their excess weight around their middle (“apples”) have more visceral fat and this type of fat is much more dangerous than the fat under our skin (called “sub-cutaneous fat”) because it is found around the heart, liver, pancreas and other organs and increases the risk not only of cardiovascular disease, but also Type 2 Diabetes and hypertension.

People who’s hips are much wider than their waist (so-called “pears”) have less visceral fat and therefore lower risk of these weight-related health problems.

Conicity Index

Conicity Index(CI) is a little more cumbersome a calculation than either Waist-to-Hip (WHR) Ratio or Waist-to-Height (WHtR), but was found in the 2015 study mentioned above with 3200 subjects to be a strong predictor of cardiovascular risk.

Conicity literally means “cone-shaped” and determines how much our  body fat distribution like two end-to-end cones.

In the first figure below, body weight is distributed evenly, however when someone has a conical distribution, their weight is more heavily distributed around the abdomen. As a result, it has increased conicity and is more highly correlated to increased cardiovascular disease (as well as Type 2 Diabetes and hypertension).

For those who are interested in calculating Conicity Index (CI), the formula is below along with the formula for Waist-to-Hip (WHR) Ratio, Waist-to-Height (WHtR).

Indices of central adiposity

Final Thoughts…

Given the sample size of the data on which Waist-to-Height (WHtR) is based (300,000 adults) and that it is an easy to determine and robust measure of cardiovascular risk, this is the one I tend to favour.  That said, Waist-to-Hip (WHR) Ratio was previously used for years and found to be a simple and accurate predictor of risk. From that point of view, either could be used, but why not both?

In my clinical experience, I have encountered many people with much wider hips than waist (so-called “pears”) but whose Waist-to-Height (WHtR) is considerably greater than 0.5, and for this reason I tend to put more credence on Waist-to-Height (WHtR) than Waist-to-Hip (WHR) Ratio as a measure of visceral fat and increased cardiovascular risk.

Since both Waist-to-Height (WHtR) and Waist-to-Hip (WHR) Ratio are very easy to determine, for those with a family risk of cardiovascular disease, Type 2 Diabetes or hypertension, I think it makes sense to aim for a waist measurement that is within both of these easily obtained measures.

Do you have questions about how I can help you lower your risk of cardiovascular disease, Type 2 Diabetes or hypertension? I provide both in-person and Distance Consultation services via Skype or telephone (and remember, many extended benefits plans will reimburse for visits with a Registered Dietitian).

Please feel free to send me a note using the “Contact Me” form on the tab above to find out more.

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Rabiee B,  Motamed N, & Perumal D, et al. Conicity index and waist-hip ratio are superior obesity indices in predicting 10-year cardiovascular risk among men and women. Clin. Cardiol. 38, 9, 527–534 (2015)

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

New Study – More Animal Fat Consumption less cardiovascular disease

INTRODUCTION: A brand new study published last week in Nutrients looked at health and nutrition data from 158 countries worldwide and found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease. As well, the study found that high carbohydrate consumption, particularly as cereals and wheat was most associated with the risk of cardiovascular disease. Significantly, both of these relationships held up regardless of a nation’s average national income.

Data from this study adds to the mounting evidence from 8 recent meta-analyses and systemic reviews of randomized control trials (RCT) summarized in this article that did not find an association between  saturated fat intake and the risk of heart disease[1-8]. It also supports evidence from the recent global PURE (Prospective Urban and Rural Epidemiological) study published in The Lancet this past December which found that those who ate the largest amounts of saturated fats had significantly reduced death rates, and that those that ate the lowest amounts of saturated fat (6-7% of calories) had increased risk of stroke [9].

Global Correlates of Cardiovascular Risk: a comparison of 158 Countries

This new study compared the average intake of 60 food items with obesity rates and life expectancy in 158 countries and found that a relationship existed between eating specific foods and raised blood pressure, death from cardiovascular disease and raised blood glucose (high blood sugar) — all of which are associated with cardiovascular disease.  The study examined nutritional data from  1993-2011 and found that total fat consumption and animal fat consumption were the dietary factors least associated with the risk of cardiovascular disease and that high carbohydrate consumption, especially as cereals and wheat was the dietary factor most associated with the risk of cardiovascular disease [10].

These findings add to the mounting evidence which calls into question whether dietary saturated fat is related to heart disease.

Total Cholesterol and Cardiovascular Risk

The present study found that eating animal fat and animal protein raised total cholesterol, however total fat and animal protein consumption were found to have a very impressive negative relationship with cardiovascular death in the European data, and a moderately negative relationship to cardiovascular death, worldwide. That is, the more total fat and animal protein eaten, the lower cardiovascular death rates were.

Often in studies,  the assumption is that high LDL is linked to risk of cardiovascular disease – not that there is a direct relationship between animal / saturated fat and cardiovascular disease.  That is, high LDL is a surrogate marker of cardiovascular disease. But does that assumption hold weight?

Perhaps a better question is “which LDL”? Small, dense LDL cholesterol  which easily penetrates the artery wall is associated with heart disease [11,12,13,14], but the large, fluffy LDL cholesterol is not [15,16], so studies seeking to impute LDL as the cause of cardiovascular diseasee need to differentiate between these LDL particles.

As well, total cholesterol is made up of the different sub-particles of LDL cholesterol, HDL cholesterol, VLDL cholesterol and triglycerides (TG), so lumping them all in together as ‘total cholesterol’ doesn’t tell us anything about risk of cardiovascular disease. We know that dietary saturated fat consistently raises the “good” HDL-cholesterol — which moves cholesterol away from the arteries and back to the liver where it can either be re-used or eliminated [17,18], so higher saturated fat intake will raise “good” HDL cholesterol, which in turn will raise total cholesterol. Total cholesterol going up is not a ‘bad’ thing.

What is important is not that total cholesterol went up but that along with increased total cholesterol, cardiovascular disease went down.

Higher Blood Sugar Associated with Higher Consumption of Cereals and Wheat

One finding of this study was that higher blood sugar (a known risk factor for cardiovascular disease) was most strongly associated with indicators of obesity such as high body mass index (BMI). What was new however is that higher consumption of cereals, especially cereals and wheat was associated with higher cardiovascular disease.

Researchers remarked that such results were not surprising “because the links between raised blood glucose, obesity, type 2 diabetes and cardiovascular disease are well established [19]”.

“…regardless of the statistical method used, the results always show very similar trends and identify high carbohydrate consumption (mainly in the form of cereals and wheat, in particular) as the dietary factor most consistently associated with the risk of CVDs.

High carbohydrate consumption, particularly as cereals and wheat was the dietary factor most consistently associated with the risk of cardiovascular disease.

Researchers looked at a maximum number of potentially significant variables and compared them to results across different regions and time periods and while they acknowledged that the accuracy of the data from developing countries may be lower, the global results that they found confirmed their earlier 2016 study data from European data only which found a significant link between cardiovascular disease and high carbohydrate consumption [20].

Of significance, the above associations held up regardless of a nation’s average national income.

Given these finding support those of the PURE epidemiological study [9] would lend support the notion that one can compare data between countries of substantially different level of income (as the PURE study did) and that high-carbohydrate and low-fat diets are not necessarily associated with poverty, as claimed [21].

The PURE study findings and those of this present study challenge the very basis of the long-standing ‘diet-heart hypothesis’ and it certainly results in some uncertainty as to what constitutes a healthy diet.

In my view, what is needed are some well-designed randomized controlled trials to determine if saturated fat intake is directly associated with cardiovascular disease – and not associated with a surrogate marker, such as LDL cholesterol.

Purported Weakness of the Data

Self-reported food-frequency questionnaires on which this study is based have long been criticized as being unreliable, however it is important to note that in the United States the NHANES Dietary Data and the Continuing Survey of Food Intakes by Individuals (USA) has also collected data using food-frequency questionnaires and such data is used as the “cornerstone to inform nutrition and health policy” [22].

In Canada, the Canadian Community Health Survey (CCHS) relies on a 24-hour recall data which is known to researchers to result in under-reporting of food intake, especially among those with a high BMI and with adolescents [23].  Given that the 2017 Obesity Update found Canada among its most overweight countries — with 25.8% of the population aged 15 and over considered obese [24], the CCHS data becomes less and less reliable, as obesity rates continue to climb.

Enduring Belief – despite recent evidence

The results of this most recently published study embody the same findings as the recent global PURE (Prospective Urban and Rural Epidemiological) study [9] publish this past December in The Lancet which found a link between raised cholesterol and lower cardiovascular risk.

This study also confirms the findings of the eight recent meta-analysis and systemic reviews of randomized control trials (RCT) summarized in the previous article which did not find an association between saturated fat intake and the risk of heart disease [1-8].

Yet, in spite of recent robust evidence there is an enduring belief that ‘saturated fat causes heart disease’ — a belief which has influenced nutrition guidelines in both the US and Canada for 40 years (since 1977).

As elaborated on in a recent article, it is now known that the ‘diet-heart hypothesis’ originated by Ancel Keys and supposedly confirmed in his ‘Seven Countries Study’ omitted known data from 22 available countries  and that when all countries were factored in there was a great deal more scatter showing a much weaker relationship between dietary fat and death by coronary heart disease than was suggested by Keys’s data.

Also as covered previously, it has been known since December 2016 that the three Harvard researchers who vindicated sugar as the cause of heart disease and blamed dietary fat — were funded by the sugar industry and that one one of those 3 researchers, Dr. DM Hegsted contributed to and edited the 1977 US Dietary Guidelines which embodied his findings of 10 years earlier, advising Americans to reduce their intake of saturated fat and cholesterol in order to reduce their risk of heart disease.

Also covered in a previous article, Canadian Dietary Recommendations regarding dietary intake of saturated fat were based on ‘health claim assessments’ conducted by Health Canada in 2000 (18 years ago) titled Dietary Fat, Saturated Fat, Cholesterol, Trans Fats and Coronary Heart Disease which was based on the US literature available from 1993-2000 and which concluded that a health risk exists between saturated fat and heart disease.

Given all of the factors mentioned above, it is my conviction that before the American and Canadian governments revise their respective national Dietary Guidelines what is needed is for them to conduct a long-overdue external, independent scientific review of the current evidence for the enduring belief that saturated fat contributes to heart disease.

If you have questions as to how I can help you live a low carb lifestyle, please send me a note using the “Contact Me” form located on the tab above.

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
  2. Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)
  3. Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406
  4. Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4
  5. Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)
  6. Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749
  7. Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353
  8. Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30
  9. Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
  10. Grasgruber P, Cacek J, Hrazdira E, et al, Global Correlates of Cardiovascular Risk: A Comparison of 158 Countries, Nutrients 201810(4), 411.
  11. Tribble DL, Holl LG, Wood PD, et al. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189–99
  12. Gardner CD, Fortmann SP, Krauss RM, Association of Small Low-Density Lipoprotein Particles With the Incidence of Coronary Artery Disease in Men and Women, JAMA. 1996;276(11):875-881
  13. Lamarche B, Tchernof A, Moorjani S, et al, Small, Dense Low-Density Lipoprotein Particles as a Predictor of the Risk of Ischemic Heart Disease in Men, 
  14. Packard C, Caslake M, Shepherd J. The role of small, dense low density lipoprotein (LDL): a new look, Int J of Cardiology,  Volume 74, Supplement 1, 30 June 2000, Pages S17-S22
  15. Genest JJ, Blijlevens E, McNamara JR, Low density lipoprotein particle size and coronary artery disease, Arteriosclerosis, Thrombosis, and Vascular Biology. 1992;12:187-195
  16. Siri-Tarino PW, Sun Q, Hu FB, Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, The American Journal of Clinical Nutrition, Volume 91, Issue 3, 1 March 2010, Pages 502–509
  17. Mensink RP, Zock PL, Kester A, Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, The American Journal of Clinical Nutrition, Volume 77, Issue 5, 1 May 2003, Pages 1146–1155
  18. Toth PP, The “Good Cholesterol” – High Density Lipoprotein, Circulation 2005;111:e89-e91
  19. Després, J.P.; Lemieux, I.; Alméras, N. Abdominal obesity and the metabolic syndrome. In Overweight and the Metabolic Syndrome; Springer: New York, NY, USA, 2006; pp. 137–152
  20. Grasgruber, P.; Sebera, M.; Hrazdira, E.; Hrebickova, S.; Cacek, J. Food consumption and the actual statistics of cardiovascular diseases: An epidemiological comparison of 42 European countries. Food Nutr. Res. 201660, 31694.
  21. Sigurdsson, AF, The Fate of the PURE Study – Fat and Carbohydrate Intake Revisited, Doc’s Opinion, October 16 2017,  www.docsopinion.com/2017/10/16/pure-study-fats-carbohydrates/
  22. Ahluwalia N, Dwyer J, Terry A, et al; Update on NHANES Dietary Data: Focus on Collection, Release, Analytical Considerations and Uses to Inform Public Policy, Advances in Nutrition, Volume 7, Issue 1, 1 January 2016, Pages 121–134
  23. Health Canada, Reference Guide to Understanding and Using the Data – 2015 Canadian Community Health Survey – Nutrition, June 2017
  24. OECD Health Statistics 2017, June 2017, http://www.oecd.org/els/health-systems/Obesity-Update-2017.pdf

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Saturated Fat and Heart Disease – Bad Fat Enduring Beliefs Part 2

This is Part 2 in the series which examines the enduring belief that dietary saturated fat causes heart disease.

INTRODUCTION: The “diet-heart hypothesis” is the belief that saturated fat and dietary cholesterol cause heart disease was first proposed by Ancel Keys in the 1950s. He encouraged Americans to reduce their fat intake by a third, while at the same time openly admitted as late as 1967 that there was little direct evidence that a change in diet would reduce the risks of arteriosclerosis [1]. As covered in the first part of this article, three Harvard researchers, Stare, Hegsted and McGrady were paid generously by the sugar industry to publish their review in the New England Journal of Medicine vindicating sugar as a cause of heart disease and laying the blame squarely on dietary fat; and in particular on saturated fatThese researchers concluded that there was “only one avenue” by which diet contributed to the development and progression of “hardening of the arteries” (atherosclerosis), resulting heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids [2].  This sounds like a very certain claim, however it is known that they lacked evidence because a year later (1968) a report from the Diet-Heart Review Panel of the National Heart Institute made the recommendation that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease – because such a study had not yet been done (see Part 1) [3].

Fast forward ten years and in 1977, one of the three researchers who was paid by the sugar industry, Dr. DM Hegsted contributed to and edited the 1977 US Dietary Guidelines [4], which embodied his findings 10 years earlier. Americans were told they should reduce their intake of saturated fat and cholesterol to reduce their risk of heart disease.

The rest, they say, is history.

The same year (1977), Canada’s Food Guide recommended that Canadians  limit fat to <30% of daily calories with no more than 1/3 from saturated fat, but did not specify an upper limit for dietary cholesterol. This was based on the belief that total dietary fat and saturated fat were responsible blood levels of LDL cholesterol levels and total serum cholesterol, not dietary cholesterol [5].

Recommendations for the continued restriction of dietary fat continued in both the US and Canada in 2015 are based on the enduring belief that lowering saturated fat in the diet will lower blood cholesterol levels and reduce heart disease.

The question is does it?

NOTE TO CANADIANS: Canadian Dietary Recommendations regarding dietary intake of saturated fat are based on ‘health claim assessments’ conducted by Health Canada which are directly tied to American research and recommendations.  Eighteen years ago, Health Canada reviewed the ‘health claim’ regarding Dietary Fat, Saturated Fat, Cholesterol, Trans Fats and Coronary Heart Disease and based on the US literature available from 1993-2000 and concluded that a health risk exists between saturated fat and heart disease, as stated here; “The effectiveness of lowering dietary saturated fat in reducing plasma cholesterol, especially low-density lipoprotein (LDL)- cholesterol, the major risk factor for CHD, is well established.” Since Health Canada’s review in 2000 (18 years ago), the link between dietary saturated fat and heart disease remains public health policy.

While it has been shown that saturated fats can raise LDL-cholesterol such a finding is meaningless unless it is specified which type of LDL-cholesterol  goes up. There is more than one type of LDL-cholesterol, small, dense LDL cholesterol which easily penetrates the artery wall is associated with heart disease [6,7,8,9], whereas the large, fluffy LDL cholesterol is not [10, 11].

Another factor that needs to be considered is that dietary saturated fat also consistently raises the “good” HDL-cholesterol which moves cholesterol away from the arteries and back to the liver, where it can either be re-used or eliminated [12,13].

What are the findings of current scientific literature?

Eight recent meta-analysis and systemic reviews which reviewed evidence from randomized control trials (RCT) that had been conducted between 2009-2017 did not find an association between saturated fat intake and the risk of heart disease [14-21].

Furthermore, recently published results of the largest and most global epidemiological study published in December 2017 in The Lancet [23] found that those who ate the largest amount of saturated fats had significantly reduced rates of mortality and that low consumption (6-7% of calories) of saturated fat was associated with increased risk of stroke.

Here is a synopsis of the findings of the eight meta-analysis and systemic reviews;

“Intake of saturated fatty acids was not significantly associated with coronary heart disease mortality” and “saturated fatty acid intake was not significantly associated coronary heart disease events”

Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled

“There were no clear effects of dietary fat changes on total mortality or cardiovascular mortality”.

Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)

“Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406

“The present systematic review provides no moderate quality evidence for the beneficial effects of reduced/modified fat diets in the secondary prevention of coronary heart disease. Recommending higher intakes of polyunsaturated fatty acids in replacement of saturated fatty acids was not associated with risk reduction.”

Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4

“The study found no statistically significant effects of reducing saturated fat on the following outcomes: all-cause mortality, cardiovascular mortality, fatal MIs (myocardial infarctions), non-fatal MIs, stroke, coronary heart disease mortality, coronary heart disease events.”

Note: The one significant finding was an effect for saturated fats on cardiovascular events however this finding lost significance when subjected to a sensitivity analysis (Table 8, page 137).

Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)

“Epidemiological evidence to date found no significant difference in CHD mortality and total fat or saturated fat intake and thus does not support the present dietary fat guidelines. The evidence per se lacks generalizability for population-wide guidelines.”

Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749

“Available evidence from randomized controlled trials (1968-1973) provides no indication of benefit on coronary heart disease or all-cause mortality from replacing saturated fat with linoleic acid rich vegetable oils (such as corn oil, sunflower oil, safflower oil, cottonseed oil, or soybean oil).”

Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353

“Available evidence from adequately controlled randomised controlled trials suggest replacing saturated fatty acids with mostly n-6 PUFA is unlikely to reduce coronary heart disease events, coronary heart disease  mortality or total mortality. These findings have implications for current dietary recommendations.”

Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30

Only one recent meta analysis conducted by the American Heart Association (by the authors of the Diet-Heart Policy for Americans, mentioned above) found a relationship between saturated fat intake and coronary heart disease, yet failed to examine cardiovascular mortality (death) or total mortality [22].

NOTE: In 1961, the American Heart Association was the author of the original policy paper recommending to limit saturated fats to protect against heart disease and therefore has a significant interest in defending its longtime institutional position.

With the exception of the American Heart Association review, the conclusion of 9 different meta-analysis and review papers of randomized control trials conducted by independent teams of scientists worldwide do not support the belief that dietary intake of saturated fat causes heart disease.


The PURE (Prospective Urban Rural Epidemiology) was the largest-ever epidemiological study and was published in The Lancet in December 2017 [23]. It recorded dietary intake in 135,000 people in 18 countries over an average of 7 1/2 years, including high-, medium- and low-income nations.  It found;

“High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.”

Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062

Those critical of the study say that it has methodological problems, including problems related to the authors dividing consumption of macronutrients (protein, fat and carbohydrate) into 4 groups (quintiles).  Some say that this is reason the data showed an inverse relationship between saturated fat and cardiovascular disease [24]. Criticisms also include that one cannot compare data between countries of substantially different level of income because “low fat consumption is very uncommon in high income countries” and that ‘the ability to afford certain foods may change the dietary pattern (e.g. high-carbohydrate and low-fat diets may be associated with poverty) [24].

Final thoughts…

Both the American and Canadian governments are currently in the process of revising their Dietary Guidelines and I feel that what is needed now is an external, independent scientific review of the current evidence-base for the belief that saturated fat contributes to heart disease.

Have questions or need support following a low carb lifestyle in a way that makes sense for you?

Please send me a note using the “Contact Me” tab above and I will reply shortly.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

 

References

  1. Keys A, Aravanis C, Blackburn HW et al. Epidemiological studies related to coronary heart disease: characteristics of men aged 40–59 in seven countries Acta Med Scand 1967 460: 1–392.
  2. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242–47
  3. The National Diet-Heart Study Final Report.” Circulation, 1968; 37(3 suppl): I1-I26. Report of the Diet-Heart Review Panel of the National Heart Institute. Mass Field Trials and the Diet-Heart Question: Their Significance, Timeliness, Feasibility and Applicability. Dallas, Tex: American Heart Association; 1969, AHA Monograph no. 28.
  4. Introduction to the Dietary Goals for the United States – by Dr D.M. Hegsted. Professor of Nutrition, Harvard School of Public Health, Boston, MASS., page 17 of 130, https://naldc.nal.usda.gov/naldc/download.xhtml?id=1759572&content=PDF
  5. McDonald BE, The Canadian experience: why Canada decided against an upper limit for cholesterol, J Am Coll Nutr. 2004 Dec;23(6 Suppl):616S-620S.
  6. Tribble DL, Holl LG, Wood PD, et al. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189–99
  7. Gardner CD, Fortmann SP, Krauss RM, Association of Small Low-Density Lipoprotein Particles With the Incidence of Coronary Artery Disease in Men and Women, JAMA. 1996;276(11):875-881
  8. Lamarche B, Tchernof A, Moorjani S, et al, Small, Dense Low-Density Lipoprotein Particles as a Predictor of the Risk of Ischemic Heart Disease in Men, 
  9. Packard C, Caslake M, Shepherd J. The role of small, dense low density lipoprotein (LDL): a new look, Int J of Cardiology,  Volume 74, Supplement 1, 30 June 2000, Pages S17-S22
  10. Genest JJ, Blijlevens E, McNamara JR, Low density lipoprotein particle size and coronary artery disease, Arteriosclerosis, Thrombosis, and Vascular Biology. 1992;12:187-195
  11. Siri-Tarino PW, Sun Q, Hu FB, Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, The American Journal of Clinical Nutrition, Volume 91, Issue 3, 1 March 2010, Pages 502–509
  12. Mensink RP, Zock PL, Kester A, Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, The American Journal of Clinical Nutrition, Volume 77, Issue 5, 1 May 2003, Pages 1146–1155
  13. Toth PP, The “Good Cholesterol” – High Density Lipoprotein, Circulation 2005;111:e89-e91
  14. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
  15. Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)
  16. Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406
  17. Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4
  18. Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)
  19. Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749
  20. Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353
  21. Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30
  22. Sachs FM, Lichtenstein AH, Wu JHW et al, Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association,  Circulation. 2017 Jul 18;136(3)
  23. Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
  24. Sigurdsson, AF, The Fate of the PURE Study – Fat and Carbohydrate Intake Revisited, Doc’s Opinion, October 16 2017,  www.docsopinion.com/2017/10/16/pure-study-fats-carbohydrates/

Note: References 11-23 were from a document prepared by the Nutrition Coalition

Special thanks to Dr. Carol Loffelmann and Dr. Barbra Allen Bradshaw of The Canadian Clinicians for Therapeutic Nutrition for their tireless research.


Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.