State of the Art 2017
The hallmark
of good healthcare is that it is “evidence-based”. This simply means that decisions in care and
preventative strategies are largely based on quality scientific evidence rather
than empirical information. This is not
to say that empirically based knowledge, that based only on practical
experience, is not important but that scientifically derived evidence tends to
be more accurate in the long run.
Regarding
diet, we are emerging from 3 to 4 decades of “this seems to make sense”, rather
than evidence-based decision making.
Unfortunately, the common advice has proven quite inaccurate and
somewhat contributory to the greatly increasing rates of some chronic diseases
such as diabetes.
Given the above
state, I thought it was appropriate to celebrate “National Nutrition Month”
with a look at the evidence-based knowledge that we have concerning the
relationship between diet and disease.
The most striking realization has been that the low fat focus of the
past 30-40 years has not only been ineffective in preventing the chronic
diseases it was touted to be a solution for, it actually has been contributing
to the increased development of most of these very diseases. There are several reasons for this:
·
Low fat means higher carbohydrate
·
A low fat diet has never been shown to lower blood lipids
·
The low fat/high carb diet causes greater weight gain than comparative
diets
·
The low fat/high carb diet causes a greater shift to a disease-causing
blood lipid pattern
A little background
is necessary to understand this important error that cost Western Nations 30
years of good dietary understanding. In the
1950’s a physiologist named Ancel Keys reported that in his study of seven
western countries, a higher total and saturated fat diet was associated with
greater heart disease risk. The problem was that Keys actually studied data
from 29 countries but “proved” his theory only reporting that from 7 countries
and omitting that from the 22 countries (76%) that found no relationship. Extensive scientific review has now found this
study inaccurate and misleading:
“There
is now probably unanimous consensus in the scientific community about this
study - it is faked, since Dr. Keys cherry picked just 7 countries. He had data
of 22, and when statistical methods are applied - there is no significant
relationship between dietary fat consumption and heart disease.”
The reasons
why the medical community, which prides itself as being “evidence-based”,
dispensed erroneous advice for 3-4 decades are complex. They are generally looked at as the top
source of nutritional advice for disease prevention, yet many studies examining
their training and ability to do this suggest otherwise.
A study
published in 2006 of over 2300 medical students at 16 representative medical
schools found that 72% beginning medical school thought that nutritional
counseling was “highly relevant” to medical practice.(1) By their final year the number had dropped
almost in half to 46%. Only 19% thought
that they had been adequately trained to provide this advice, and only 17%
reported to doing so with their patients.
A prior study examined the knowledge of internists and cardiologists about the impact of
diet on blood lipids. Eighty-four
percent of cardiologists and 96% of internists did not know that a low fat/high
carb diet would raise blood triglyceride levels. Similarly, 70% of cardiologists and 77% of
internists did not know that this diet would lower HDL, or good cholesterol.
The problem is
that medical education is devoid of nutritional education instead focusing on
other areas of concentration. Nutrition
science has not filtered into that training, yet the public perception is that
this is where nutritional advice should be available.
This domain
should default to specifically trained individuals well versed in nutritional
science, but many barriers to this remain in the system.
The thought
process that has led to the standard low fat diet advice for the past 3-4
decades was an oversimplified assumption that the fat responsible for arterial
plaque must be generated by dietary fat. However, the higher carbohydrate dietary
pattern that this assumption created actually causes a more risky shift in
blood lipid patterns than does a higher fat, lower carbohydrate pattern.
In reality,
any energy in excess of immediate need is sent to the liver to be converted to
fats as that is the primary energy storage form that humans use. The sugars from a higher carbohydrate diet
have been shown to increase liver triglyceride production, lower HDL
production, increase LDL or bad cholesterol production and cause a shift in the
LDL particle size to a smaller, more plaque-forming variety. This combination of changes is the one that
causes the greatly increased vascular disease risk in diabetics.
The increase
in LDL production associated with a higher carb diet occurs because this diet
causes higher insulin levels. Making
cholesterol in the liver requires energy availability, and insulin is a potent
signal of energy availability.
Most major
bodies that set guidelines about dietary behavior have recently revised their
positions stating that the dietary high fat hypothesis has not proven
true. They also suggest that the low fat
diet preoccupation has pushed us to a higher carbohydrate diet that has been a potent
driver of the obesity and diabetes epidemic.
Diabetes is of
particular concern as vascular complications remain the dominant cause of
associated disease and deaths. Fuel to
this concern was added recently by a study that looked at carotid artery
plaques in obese and non-obese subjects.
While high dose statin therapy lowers plaque volume by 4.2% in non-obese
subjects, obese subjects had it increase 4.8% in 12 months despite lowering of
LDL.(3) Other factors besides LDL
contribute to plaque formation including inflammation and glycation, or direct
sugar damage to tissue.
The lesson to
deduce from the evidence-based look at the current research on diet and disease
is that we are generally ill suited to the dietary pattern of the last 30 to 40
years. While humans thrived on a diet of
about 30% protein, 40% fat and 30% complex carbohydrate for the first 6 million
years, the current shift to 15% protein, 25% fat and 60% carbohydrate has
resulted in growing rates of a number of chronic diseases that have a metabolic
basis. The high percentage of total carbohydrate has been further complicated
by the dominant amount being refined and with added simple sugars.
So the
knowledge base we have concerning diet in 2017 looks very different from the
commonly recommended dietary pattern of the last 40 years. Now we face the difficult task of actually
implementing that change, but the motivation is that the stakes are high.
1) Spencer et
al. PREDICTORS OF NUTRITIONAL COUNSELING
BEHAVIORS AND ATTITUDES IN U.S. MEDICAL STUDENTS. Am J Clin Nutr, 2006;84:655-662.
2) Flynn et
al. INADEQUATE PHYSICIAN KNOWLEDGE OF
THE EFFECTS OF DIET ON BLOOD LIPIDS AND LIPOPROTEINS. Nutri J, 2003;2:2-4.
3) Sandfort et
al. OBESITY IS ASSOCIATED WITH
PROGRESSION OF ATHEROSCLEROSIS DURING STATIN TREATMENT. J Am Heart Assoc, 2016;5:e003621.
