Medical News story on a Poster
Presentation at the American Diabetes Association (ADA) 2014 Scientific
Sessions in San Francisco made an important, but unstated, point. The “new,
real-world study,” the report said, “based on real clinical practice,”
demonstrated “a very strong effect” of glycemic control on cardiovascular
outcomes.” The lead author of the study was a professor of epidemiology and
biostatistics at University College London.
The lede for the Medscape piece was, “Among patients with Type 2 diabetes who
start taking insulin, those who attain good glycemic control are less
likely to have a major adverse cardiac event (MACE) in the medium term than
those who fail to achieve this.” But the unstated point was that
“it doesn’t appear to matter how
you get to (glycemic) control; it’s getting to control that matters.”
The message was to “achieve improved HbA1c…by whatever means.”
“The study covered nearly 3,000
patients who had had diabetes for about 9 years but had hyperglycemia despite
generally receiving oral antidiabetic agents.” That’s like me, before starting
a low-carb diet. “The patients had a mean age of 61, about half were women, and
at baseline they had a median body mass index of 28.6.” Despite taking up to 3
oral antidiabetic agents [again, like me], their median HbA1c was 9.3% (range
8.1 – 10.7%). These patients were relying solely on their doctors to manage
their Type 2 diabetes. The result: their disease had progressed to the
point where their doctors HAD to start them on insulin.
So, what happened? “Patients whose
HbA1c levels remained high had worse outcomes.” How much worse? 25% worse.
“Specifically, a 1% higher HbA1c increased the risk of a major
adverse cardiac event (MACE) during a 4-year follow-up by 25% compared with
an otherwise similar patient with a 1% lower A1c.” The “1% increase in HbA1c above
the mean was associated with a significant 36% increased risk of a first
stroke, and a significant 31% increased risk of cardiovascular death.
During the study
follow-up, there were 44 nonfatal MIs (myocardial infarctions, or heart
attacks), 57 nonfatal strokes, and 60 deaths from cardiovascular causes. There
were 148 deaths from all causes.”
Seven percent were not taking any
oral antidiabetic agents when they began insulin therapy. About a quarter were
taking 1, half of the patients were taking 2, and a fifth were taking 3 orals.
Two thirds of the patients were taking Metformin, three-quarters a sulfonylurea
(!), twenty percent were on a TZD, and the rest on other diabetes meds.
“The patients made substantial gains
in glucose control,” the lead author said. “The median HbA1c dropped to 7.4%
(range 6.7% – 8.4%) at 1 year and remained around that level at years 2, 3 and
4.” “The results confirm that people with better blood glucose control have
better cardiovascular outcomes,” the author said.
The guided-poster-tour moderator told
Medscape Medical News, “This study
suggests (that) getting glycated hemoglobin down with low-dose insulin in
combination with other therapies is safe and might be beneficial by reducing CV
events.” That’s a safe conclusion! He added, “Although it was not a prospective
study with a comparator arm, nevertheless it reinforces that ‘good
glycemic control is important to prevent cardiovascular events.’”
Not surprisingly, this study was
funded by Sanofi, a manufacturer of insulin (Lantus and Apidra), So, the
outcomes benefited them by promoting the use of “low-dose insulin in
combination with other therapies.” But remember the takeaway: “It doesn’t appear to matter how you
get to (glycemic) control; it’s getting to control that matters.”
Unfortunately, this study did not consider
dietary choices as part of their diabetes care. But
neither did it exclude diet. It doesn’t matter how you get control;
it’s getting control that matters. In this study, the patients
relied on their doctors to take care of them, and they “had had diabetes for
about 9 years but [still] had hyperglycemia [high
My Fasting Blood Sugars, after 16 years of letting my doctor prescribe
progressively more anti-diabetic meds (3 total), and doing nothing on my own behalf,
was still in the 150s. Like these patients, I was on the verge of injecting
insulin. But here’s the critical difference: instead of insulin, my
doctor started me on a Very Low Carb diet. I not only lost a great
deal of weight, I had to discontinue most of my antidiabetic meds to avoid hypoglycemia
(low blood sugar)!
I keep hoping that someday I will
read in the scientific or mainstream media that eating a low-carb diet will
reduce the risk for Type 2 diabetes. I mean, it’s so obviously true that I am
at a loss to explain why I don’t read it all the time. Then, a recent Diabetes in Control headline gave me
renewed hope, until I saw the source and read the story.
The headline, ADA: Improving Quality
of Diet Reduces Risk for Type 2 Diabetes, had me hopeful. The sub-title,
“Consuming healthier foods improves risk independently of other lifestyle
changes such as weight loss or physical activity,” gave me further
encouragement. Then, my hopes crashed.
The story began, “Researchers at the
Harvard School of Public Health have found that patients who ate more whole
grains, fruits, vegetables, and less sweetened beverages and saturated fats
improved their diet quality index scores by ten percent over four years. This
reduced their risk for developing Type 2 diabetes by about 20% when compared to
those who made no diet changes.” The “control” ate the Standard American Diet
(SAD), which is filled with junk food.
The measurement tool that the Harvard
“researchers” used was the “110-point Alternate Healthy Eating Index 2010”
(AHEI). Harvard’s Walter Willett and colleagues developed the AHEI in 2010 to
“improve on” the Healthy Eating Index (HEI) that was originally developed by
the USDA in 1990 and updated every five years to conform to the changes in the
USDA’s Dietary Guidelines for Americans. It measures diet quality as a function
of conformance to the Guidelines.
A comparison of Harvard’s AHEI and
the USDA’s HEI can be viewed on Yahoo. The Yahoos site’s main value, however,
is that it provides links to both the 2010 AHEI and the HEI. In my view,
obviously, the AHEI and HEI are both deeply flawed, not least
for their views about fats, especially liquid fats (refined “vegetable” oils) made
from polyunsaturated sources (corn, soy bean, sunflower, peanut, canola and
others). In addition, both Harvard’s AHEI and the USDA’s HEI regard a “move to
a plant-based diet” an “important step in the right direction,” according to
the AHEI link. They would have you view “solid” (saturated) fats as harmful,
and severely curtail your consumption of egg yolks, butter and red meat.
Harvard is still hopelessly hamstrung by its Hammurabian bias. This latest
“study” simply seeks to promote the “ancient” (50-year old) and totally
erroneous bias against saturated fats.
The USDA’s Center for Nutrition
Policy and Promotion [note the undisguised use of ‘promotion’ here] uses
data collected via 24-hour recalls of dietary intake in national surveys
to construct the HEI score. The methodology of Harvard’s 110-point AHEI uses “a
scoring system similar to the USDA’s index…using information about daily diets
collected from more than 100,000 female nurses and male health professionals
taking part in two long-term studies.”
Harvard can’t be faulted for wanting
to improve or replace the “one-size-fits-all” Dietary Guidelines for Americans.
But just tweaking it, as Harvard does, is not the solution. Neither, however,
do I fault some of Harvard’s tweaks. My main gripe is with their confounding of
“more whole grains, fruits, vegetables,” with “less sweetened beverages and
saturated fats.” And, in this last phrase, the conflating of “sweetened
beverages and saturated fats.” Elsewhere, they (and the USDA) consistently
conflate “saturated fats” and “trans fats.” These are egregious examples of
using a rhetorical device to confuse and mislead the public. And it is
downright damnable. Damnable, I say.
With respect to this particular
“study” and public policy press release, how can Harvard say that the 10%
improvement in diet quality index scores (over those who made no self-reported
diet changes), and which lead to a 20% reduction in developing Type 2 diabetes,
was attributable to reporting eating “more whole grains, fruits, vegetables,” or eating “eating less sweetened
beverages and saturated fats.” Perhaps the 10% improvement in scores was
attributable to the (self-reported) elimination of sweetened beverages without
any change in saturated fat intake or whole grains, fruits and vegetables. Or
eating more whole grains, fruits and vegetables and fewer sweetened beverages,
but the same amount of saturated fat. Or any combination. But that’s
epidemiology, a very weak “science,” at best.
But that’s about what I expected when I read that this “study” was a
product of the Harvard School of Public Health. It is simply a promotional
piece to advance their idea of a
“healthy diet.” A perfect example of confirmation bias.
The full title of this Medscape Medical News story is, “Diabetic
Foot: A Cinderella Condition, Needs a Team Approach.” The simple title,
“Diabetic Foot Needs a Team Approach,” would have been much better, but would
get fewer “clicks.” It was actually a good story. The findings were reported at
the ADA’s 2014 Scientific Session. The key takeaways:
is a need for a “uniform, multidisciplinary approach,” with a “national
treatment plan” for diabetic foot. To this end, a U.S. National Diabetic Foot
Registry is now being established. (All four commenters agreed).
one large “safety-net hospital system that serves a diverse patient
population,” in “2000 there was nearly a 50-50 chance that if you came in with
a diabetic-foot infection, you would lose your foot.” As a result of their establishing
a limb-salvage program, there has been a staggering reduction in the number of
average age of the amputee population was 55.9 years, 72.5% of the patients
were male, and the average H1c was 9%. Seventy percent of the patients had
coronary artery disease, and 14% end-stage renal disease.
was “a robust independent predictor of death, associated with a significant,
almost 85% increased risk for mortality,” with “most of the deaths – just under
50% -- due to cardiovascular disease.”
minor amputations were associated with an almost 50% increased mortality risk,
a somewhat surprising finding.” And, “Once you have an amputation, you go down
a not very healthy road.”
The session moderator told Medscape Medical News, “It
was…disappointing... to see that minor amputations had no better outcome – you
would expect that they would do better, but apparently not.” “But I think that
if you look at the natural course of the disease, these patients die of
cardiovascular disease – it doesn’t matter what you do to their extremity. They
all die of CVD. I guess we should expect it, but we would hope it would be
better,” he said. Wow!
Given this dismal, if no longer
abysmal outlook, I would hardly call this a “Cinderella Condition.” Even having
the amputation rate fall from 36% to 11%, after the limb-salvage program was
implemented at that particular safety-net hospital system, “They all die of
CVD” is not a story-book
ending. It’s not like “they lived happily ever after,” unless it is to be
inferred, that the prospect of
going forward with a “uniform, multidisciplinary approach” and a “national
treatment plan” for diabetic foot has the potential
for “a Cinderella ending.” I’ll try to imagine that that is what was intended
by the title.
I haven’t written about diabetic foot
before except to mention that diabetic neuropathy (the cause
of “diabetic foot”), along with nephropathy and retinopathy, are
the three major classes of diabetic Microvascular Complications, as well
the seldom mentioned erectile dysfunction (ED). Cardiovascular
disease (CVD) – as in “They all die of CVD” – is the major Macrovascular
Complication of Type 2 diabetes. Hopefully, your A1c is much, much
lower than 9%. That average glucose (eAG) of 212mg/dl requires drastic action
on the part of both the physician and the patient.
Of course, if you’ve somehow just
been diagnosed with diabetes and have an A1c as high as 9% (or higher), you can do something dramatic to
lower it. One thing you undoubtedly will do, and are doing, is your homework.
If the doctor hasn’t scared the bejesus out of you, reading about the
progressive nature of this disease, if you follow “usual care,” is scary enough.
Reading about the complications and the likely prognosis
is ever scarier. Reading the five bullets above is downright terrifying. But
you can do your homework and choose a course of action to avoid all of this.
The first A1c that I ever had, long
before that test was common, was given to me by an endocrinologist 26 years ago
in 1993. My A1c was 8.9%. Curiously – inexplicably, really – I didn’t have
another A1c test for 10 years, and by this time I had already been on a Very
Low Carb diet (20 grams a day) for almost a year. My A1c was then 5.4%. I would
love to have known what it was just before I began to eat Very Low Carb. It would
certainly have been “out of control.” My FBS’s were in the 150s and I was maxed
out on 2 oral anti-diabetes meds and starting a 3rd.
My editor says that I was very lucky.
I sometimes forget. Many people develop early signs of complications in just a
few years of “uncontrolled glucose control.” Others not. I guess I was, and
continue to be, lucky. Do you want to take a chance that you’ll be lucky too?
Are you a gambler? Just be aware: Diabetes Foot is NOT a Cinderella
“Adding Insulin to Metformin for T2s
May Increase Risk of Death,” was a scary headline of a 2014 Diabetes in Control article about a JAMA paper: “Association between Intensification of
Metformin Treatment with Insulin vs. Sulfonylureas and Cardiovascular Events
and All-Cause Mortality Among Patients with Diabetes.”
Both the Diabetes in Control piece
and the JAMA paper were qualified and raised more questions than they answered.
In my mind, so did the objectives and design of the study. Why, for example,
would anyone today want to
compare adding insulin to adding a
sulfonylurea? Haven’t the sulfonylureas as a class been thoroughly
discredited? I cite Dr. Ralph DeFronzo’s Banting Award keynote address to the 2008 ADA Convention in San Francisco and
his paper published in Diabetes in
which he wrote, “Sulfonylureas are not
recommended because, after an initial improvement in glycemic control, they are
associated with a progressive RISE in A1c and a progressive LOSS of
The “Adding Insulin…” study took
place in the Veterans Administration (VA) hospital system in Nashville. The Vanderbilt University researchers
reported more patients in the sulfonylurea cohort than in any other. (“Among
178,341 Metformin monotherapy patients, 2,948 added insulin and 39,990 added a
sulfonylurea.”) That reminds me of the story of the person who lost a ring in a
dark alley and was looking for it under a street light. When asked why, he
replied, “There’s more light here.” But couldn’t they have used a more current
treatment modality than a sulfonylurea, like a GLP-1 (or today a SGLT-2), rather
than one that causes more harm than good to the patient?!
The Objective of the study was
alarming in itself: “To compare time to acute myocardial infarction (AMI),
stroke or death in a cohort of metformin initiators who added insulin or a
sulfonylurea.” They quickly dispel this most alarming outcome objective: “Acute
myocardial infarction and stroke risks were statistically similar.”
Whew! That’s the good news. The bad
news? The Conclusion (from the full-paper): “Among patients with diabetes who are receiving Metformin, the
addition of insulin compared with sulfonylurea was associated with an increased
risk of a composite of nonfatal cardiovascular outcomes and all-cause mortality.”
Of course, this finding of an
“association” was followed by, “These
findings require further investigation to understand risks associated with
insulin use in these patients…” Okay, that’s pretty much pro-forma these days. It also just a
plea for more taxpayer funding for further investigations (a medical school’s
research department jobs program). But that final sentence of the Conclusions
section has a compound predicate; it continues, “…and call into question recommendations that insulin is equivalent
to sulfonylurea for patients who may be able to receive an oral agent.”
Okay, okay, but even in 2014 sulfonylureas weren’t
the only oral agent available! And they overwork the remaining working beta
cells that you have, leading to their destruction! Go back and read Dr.
Sulfonylureas have been in use in the
U.S. since the late ‘40s. Metformin was introduced in Britain in 1958, in
Canada in 1972, and finally permitted by the FDA in the US in 1994. Now, it is
the preferred first course of treatment both in Europe and the U.S. for
pre-diabetes and is used as a
monotherapy by many T2s (like me), who rely primarily on diet for blood sugar
control. But if I needed a 2nd therapeutic, I WOULD NEVER
AGAIN AGREE TO TAKE A SULFONLUREA (Micronase, glyburide, glipizide, etc.),
just as I would never agree to take a statin to lower my Total Cholesterol and
LDL-C. Both my doctor and I are very happy with my lipid (cholesterol) levels
as they are, thank you very much.
So, where do we go from here? It’s
confusing. The first “Practice Pearl” in Diabetes in Control raises a
very good issue: “Many variables were not considered in choosing the
participants in this study.” Their takeaway: “These findings require further
investigation to understand risks associated with insulin use in these
patients.” Yes! More studies!
But it comes as no surprise to me that the VA is still administering
sulfonylureas; or that the researchers at the Vanderbilt University Department
of Medicine, Department of Biostatistics, and Department of Health Policy
continue to advocate for that particular “oral agent” (a sulfonylurea). It is
dirt cheap. And insulin, especially since this was originally published in
2014, has become really expensive. But isn’t that what drives our
national health policy today?
The day after the 2nd of
the last two bombs dropped in my inbox (see Retrospective #221), another one
“exploded.” “Better Diabetes Self-Management with Cognitive Therapy,” is a Medscape Psychiatry Minute by Dr. Peter
Yellowlees. As my readers know, I believe that self-management of Type 2
diabetes should be advocated by physicians and in the medical
literature. Patients should be more involved in their own Type 2 diabetes care.
So, what was this all about?
The video synopsis, with accompanying
transcript, “A randomized controlled trial of cognitive behavioral therapy for adherence
and depression (CBT-AD) in patients with uncontrolled Type 2 diabetes,”
appeared in Diabetes Care. Note: “adherence and depression.” The work, with 87 adults, was done at Massachusetts General
Hospital in Boston.
It was an expensive, randomized
controlled intervention in a hospital environment, with a “usual care”
component and a predictable outcome: the intervention group (depressed patients
with uncontrolled Type 2 diabetes), received CBT and, after 4-, 8-, and
12-month follow-up time points, “maintained 24% higher medication adherence,
17% greater adherence to self-monitoring of blood glucose,
and lower A1c values.” The “better” adherence outcome was
not surprising, but what interested me was the outcome that, “…both groups being less depressed.”
Hmmm. Both groups took
their pills, monitored their blood glucose and had A1c tests, and both groups ate
the same horrible hospital food,
so presumably the adherence end-points and A1c improvements of the
intervention group were a result of their CBT treatment therapy.
And because both the intervention and control groups saw themselves as
receiving this expensive “care,” both groups came out less depressed!
Well, that’s good for both patients and the psychiatrists who, after all, needed
to feel that they’re helping patients, not least to justify the cost of the
Not to put too fine a point on it, in
the ABSTRACT the only mention about depression was this: “For depression, there
was some evidence of continued improvement post-treatment, but no between-group differences.”
I don’t mean to be critical of
Cognitive Behavioral Therapy. I actually think CBT is good. My main frustration
with this study is that these seriously-ill, hospitalized patients, all
with uncontrolled Type 2 diabetes, were being taught, through CBT, “adherence:”
Take you pills and test your blood regularly to see how sick you are AND
HOW MUCH SICKER YOU’RE GETTING. No wonder they’re depressed! Isn’t everyone
depressed when the medical therapy prescribed, including weight loss advice, isn’t
I guess it never occurred to these
docs (they’re psychiatrists) that Type 2 diabetes is a disease of hormonal
disregulation caused by insulin resistance arising from impaired glucose
tolerance: in other words, carbohydrate intolerance. And the most effective
treatment protocol, rather than “adherence” to a
pharmacotherapy treatment regimen, is to dramatically curtail intake of dietary
carbohydrates! (Good luck with that on hospital food!)
But that’s what I did. When, at my
doctor’s suggestion, I started to eat a Very Low Carbohydrate diet (just 20 grams
of carbs a day!), I was on three different classes of oral
anti-diabetic medications, and maxed out on two. The first day I had a hypo,
and I called my doctor. He carefully (and very
quickly, all in the first week) drastically reduced my meds. It left me
with only one, a small dose of Metformin (500mg, once a day). That was 17 years
and 150 pounds ago.
with Very Low Carb, is, for me, easy because on Very Low Carb, you’re never
hungry. Medication and self-monitoring adherence will improve too as you
will look forward to daily and weekly improvements.
I don’t need expensive therapy, although I don’t knock it. Do whatever
works for you. The important thing is
to choose the right dietary therapy for treating Type 2 diabetes.
If you’ve been diagnosed with pre-diabetes or Type 2, Learn what carbohydrates
are. Test your blood sugar regularly. “Eat to your Meter.” Your doctor and you will
both approve of the weigh-in and lab results, and you won’t need a psychiatrist
(for this), because as you lose weight and get better lab results, you will
be less depressed. Your medication (if required) and self-management adherence
will improve, at minimal cost to you and society. And your mood will be
Medscape Medical News dropped 2 bombs in my inbox last week. My post-bombing analysis is that
they both missed the target. The first was due to a navigational error and the
second due to cloud cover. That’s my analysis, anyway.
“Congratulations! We’re Making
Strides in Diabetes Care, “by Dr. Anne L. Peters, MD, CDE, a respected, establishment
diabetologist, is simply a cheerleading piece timed for the ADA convention. She
provided three links to recent articles in 1) the Journal of the American Medical Association (JAMA), 2) the Annals of Internal Medicine, and 3) Diabetes, the Journal of the American
Diabetes Association, summarizing, “This is great news. We are doing a better
job than ever.”
Would that her audience, comprised
largely of “treating” physicians (like herself,) agree? But then, maybe that’s
the point of her getting ginned up to deliver this Pollyannaish piece. I
suppose the treating physicians convened at the Annual ADA Convention are in
need of a morale boost. She and her colleagues primarily treat uncontrolled
In spite of the “strides” claimed, I
feel there must be among the vast majority of practicing physicians a
frustration, a frantic despair, in fact, a feverish frenzy over the utter failure
of the “usual care” treatment protocol, dictated by their medical associations
and their government overseers. Dr. Peter’s problem, and that of the entire
medical and public health establishment, is that they simply are using the
wrong treatment protocol (and many of them know it).
The 2nd bomb, which
appeared 2 days later, was titled “Diabetes Prevention Programs: A Waste of
Money.” This was a Medscape Interview
of Richard Kahn, PhD, Professor of Medicine, University of North Carolina,
Chapel Hill. A controversial counter message, it focused on “lifestyle
modification programs geared for weight loss,” since these programs have been
shown to “delay or prevent the onset of Type 2 diabetes.” The Medscape Editors’ note that “as many as
82 million Americans are thought to have prediabetes.” “These people”
(referring to people who had completed a “usual care” Diabetes Prevention
Program) had an enormous amount of attention given by health professionals.”
“Those interventions – almost every one – were expensive,” Dr. Kahn asserted.
And they failed.
Dr. Kahn adds: “The first thing you
see is that the overwhelming number of studies didn’t even go out to one year,”
and “the assumption the authors make” is “that that amount of weight can be
lost forever. That has simply never been seen except in bariatric surgery.”
“From a medical point of view, it doesn’t look like that initial weight loss
does much, if anything. For some clinical effect you have to lose substantially
more weight – 20%, 25% of your body…,”and, Dr. Kahn continues, “it would have
to stay off for a long time” to be a cost-effective program worthy of “society
pay(ing) for the intervention,” given “how difficult it is to keep weight off.”
So, Dr. Kahn’s “after bombing
assessment” confirms that the “usual care treatment protocol” you are likely to
receive in your clinician’s office is ineffective and the reason
why so many physicians and patients
feel frustrated. Dr. Kahn said, under such “diet and lifestyle” diabetes
prevention programs, “the assumption that the weight will be lost and held off
for life… is unrealistic.” Dr. Kahn isn’t asked about what he meant by that,
but I think I understand: his analysis of the data shows unproven tenets and assumptions;
his conclusion: the present modus operendi (a low-fat, “balanced”
diet protocol) is simply not cost-effective because it doesn’t work long-term.
But Dr. Kahn does leave a door open.
I suspect he knows anecdotally (as I know personally), that long
term, permanent weight loss is
indeed possible – if we re-program our
sights and target carbohydrates. He says, “Some people decide, ‘I’m
going to do it. They’ve invested nothing. That’s great for them, but we’re not
arguing about whether people should be encouraged to lose weight. What we’re
arguing against is having society pay the bill for this when it hasn’t been effective.” Yeah, he does
know. But, alas, the good professor can’t afford to say it. Too bad, really.
Medscape then asks, “What’s the main takeaway for clinicians, then?” Dr. Kahn’s
final remarks, “People who are overweight or obese should be strongly
encouraged by their healthcare provider to lose weight and keep it off. If a
provider feels that there is a good resource in the community, he or she should
refer the person to that resource.” Hello. Anyone listening? Check out how I lost and keep off 40% (150 pounds)of my
body weight. See Retrospectives #213 & #214.
“Eat protein to lower stroke risk” is
the title of a piece in The Telegraph.
The article is based on a study in Neurology,
“Quantitative analysis of dietary protein intake and stroke risk,” from the
Nanjing School of Medicine in China.
story begins, “Eating a high protein diet [emphasis
added] significantly lowers the risk of stroke and could prevent 10,000 deaths
in Britain every year, a study has suggested.” A high protein diet? Maybe some hyperbole
by an eager reporter, combined with bad editing. The lesson here: stories in
the popular press are not peer reviewed.
“The (total) amount of protein that
led to the reduced risk was moderate – equal to 20 grams a day,” it says. Moderate?
That’s a small amount (by American standards). The Standard American Diet (SAD,
ironically) on the Nutrition Facts Panel of manufactured and processed food
packaging calls for 50 grams a day (10 percent of total calories), and most
Americans eat a diet of more than 15 percent protein. Remember, the lower
minimum percentage in the “Dietary Guidelines for Americans” only survives
because they writers are heavily influenced by the vegan lobby who advocate a
plant-based diet to save the planet from greenhouse gasses (caused by bovine
flatulence), etc., etc.
The study RESULTS, from the ABSTRACT,
however, are more specific: “The pooled RR [relative risk] of stroke for the
highest compared to the lowest dietary protein intake was 0.80 (95% CI
[confidence interval] 0.66-0.99 [range]).” That means the risk of stroke was
4/5s as great (0.80) for the highest compared to the lowest dietary protein
The ABSTRACT had another interesting
result: In addition to the 20% relative reduction in stroke risk for overall
dietary protein intake, they reported that “stratifying by protein
type, the relative risk of stroke for animal protein
was 0.71 (95% CI 0.50-0.99).” For the mathematically challenged, that
translates to an almost 50% greater (29% versus a 20% reduction) in relative
stroke risk. In simple terms, in the words of The Telegraph’s science correspondent, “The reduced risk
of stroke was stronger for ANIMAL protein than vegetable protein.
“Consuming as little as one chicken
breast, or a salmon fillet, -- the equivalent of 20g – reduced the risk of
stroke by 20 per cent,” The Telegraph
said. The study analysis does have a bias, however. According to the study’s
lead author, “people should avoid red meat,” which has been associated with
increased stroke risk, according to The
Telegraph. “These results indicate that stroke risk may be reduced by
replacing red meat with other protein sources, such as fish” Hmmm. Isn’t pork
the “other white meat”? In any case, it appears the Brits have a vegan lobby
too; Or, if this was part of the study’s conclusions, perhaps the lead author was
pandering to the “perceived wisdom” to get published.
The bias deepens, however, in the
accompanying editorial in Neurology. The
authors review what “many experts recommend”: “…a low-fat diet such as the AHA
diet, formerly the National Cholesterol Education Program diet, based on the
evidence for an atherogenic role for fasting cholesterol levels.” That means,
you need to get Total Cholesterol (TC) below 200mg/dl (with a statin)
regardless of the lack of hard evidence to support lower TC in CVD prevention.
“However,” they say, “evidence-based
dietary recommendations for reduction of stroke risk are limited.” And then,
interestingly: “The current recommendation for monounsaturated fat instead of
saturated fat reflects the evidence that the
source of dietary fat matters
more than the proportion of calories
from fat” (emphasis added). The worm turns (in 2014) in the UK.
More evidence in the medical establishment’s thinking that the proportion of
calories from fat now matters less than the type; still a lagging
bias against saturated fat, but a green light for monounsaturated fat (olive
oil, etc.) and no mention, and
especially important, no advocacy for
polyunsaturated fats (vegetable oils like soy bean and corn oil),
which the American dietary establishment strongly advocated for in the 2015
If this sounds like the Mediterranean
diet, well, it is. The editorial then swings full speed into an incestuous
vortex of “validating the expectations of the perceived wisdom.” “Therefore,”
it concludes, “it seems invalid to focus exclusively on protein (‘Eskimo Diet’)
or what we have done with lipids in the past.” [That sounds like a mea culpa ON FAT]. “In other words,”
they say, “eating vegetables, fruits and protein every day will help to keep
stroke away!” A not very clever attempt at drollery, to be sure, but to this skeptic,
a sure sign of transition in the UK’s dietary establishment.
Not a surprising result but the term
“usual care” caught my attention in this otherwise unsurprising Medscape
Medical News piece in a special diabetes-themed issue of the Journal of the
American Medical Association, timed to coincide with an annual American
Diabetes Association (ADA) Scientific Session. These days the bariatric surgery
business in on the rise, and self-serving articles like this one are all too
common, even in peer-reviewed scientific journals.
“Usual care” is a “term of art” so commonly
used that the Medscape reviewer did not define it. It was defined in the study
itself and, I’m sure, in the practice guidelines of bariatric surgeons. Besides,
this study was not about “usual care.” It was about promoting
bariatric surgery as the preferred course of action for the treatment of obese
Medscape quotes a JAMA editor who was
also co-author of an accompanying editorial: “The study findings validate the expectations [LOL] of
bariatric-surgery-associated weight loss and provide concrete numbers to cite.”
She added, perfunctorily, “Diet and lifestyle measures will always be the
cornerstone of diabetes therapy, but bariatric surgery is an option for
patients who are unable to
lose sufficient weight with diet and exercise and who are willing to accept the risk of bariatric
surgery and comply with the lifestyle changes required after bariatric
surgery” [all my emphases].
So, let’s see what we’re being told
here: 1) “Usual care” usually doesn’t work, for most obese
diabetics; The “usual” “diet and lifestyle measures,” a “balanced, low-fat diet
and exercise,” as counseled by physicians who treat obese diabetics, are
the “cornerstones of diabetes therapy.” And when this “usual care” is
prescribed, and followed by the patient, with the resulting “insufficient”
weight loss, the patient will then be counseled to consider the option of
bariatric surgery. That is, if the patient is “willing to accept the risk of bariatric surgery and comply with the lifestyle changes required after bariatric surgery. Thanks
a lot! Maybe a change before surgery should be thought
Okay, let’s review again: “Usual
care,” as currently defined by the standards of medical practice, is such a
hopeless cause as to be forlorn. And, of course, your failure to
achieve sufficient weight loss with “usual care” is laid on YOU,
the patient, who was obviously
“non-compliant” with the diet and lifestyle measures your physician had “prescribed.” So, surgery to the rescue!
The doctor takes charge AGAIN, providing the patient is “willing to accept the risk of bariatric surgery and comply with the lifestyle
changes required after
bariatric surgery.” Is this what you want?
And the “lifestyle changes” after
bariatric surgery? Liquid meals only
for weeks or months after surgery. Thereafter, only very small meals at
frequent intervals because the stomach is no longer a large expandable storage
pouch. And if you eat more than your greatly reduced stomach capacity: nausea,
projectile vomiting, even dumping, i.e., where food gets “dumped directly from
your stomach pouch into your small intestine without being digested.” Think
Another point to bear in mind: These
“lifestyle changes” are now life-long REQUIREMENTS, not
options. In contrast, the “lifestyle changes” of a low-carb “diet and exercise”
program are volitional. If you want to, you can take a “holiday”
from them now and then, and the major downside is a temporary weight gain or
loss of blood sugar control, and guilt. After bariatric surgery, you had better
not try to take a break from your regimen; you will pay dearly for it. As a
consequence of accepting the risk of bariatric surgery, you must
comply with the lifestyle changes required after bariatric surgery. You
are no longer “the master of your fate;” you are no longer “the captain of your
Of course, none of these consequences
are necessary. You do not need to opt for bariatric
surgery. You simply need to opt for A DIET THAT WORKS
to achieve “sufficient” weight loss, permanently. Admittedly, it is also a lifetime requirement,
if you want to maintain the weight you have lost (and all the other improved
health markers) for the remainder of your lifetime – a lifetime that will
likely be longer if you do.
My regular readers know, of course,
that I personally adhere to a Very Low Carb lifestyle. And I don’t exercise. I
don’t enjoy it. You can, if you like it, or you can wait until you’ve lost 50
or 100 pounds to start an exercise program. You’ll enjoy it more and reduce
your risk of injury when it isn’t so much work to lug around that extra weight.
You could start (as I did) on a Very Low Carb regimen (20g/d),
or you could just go Low Carb, at 50 or 100 or even 200g/d.
Misleading advertising riles me all
the time, almost as much as grammatical errors by news anchors, talk show hosts
and United States Senators. And I am especially riled by advertising that
claims that others are being misleading while being themselves misleading. They
must think we’re all dummies!
My current (2014) favorite is a
teachers’ union advocating for the Common Core curriculum. In it, an actor
playing a teacher says (I’m paraphrasing), “Those opposed to the Common Core
are misleading the public”; she protests, “Common Core does NOT tell teachers HOW to teach” (emphasis mine). “THAT is misleading,” she says. What she DOES NOT say
is that Common Core DOES tell
teachers WHAT to teach!
THAT’S ITS PURPOSE. Grrrrrrrrr!
Another TV commercial I’ve heard over
and over says “Diabetes causes nerve pain.” I guess it’s a scare tactic. You’re
supposed to rush to your doctor and ask him to prescribe the drug that is being
advertised. It unnerves me
(hehe) to hear it. Diabetes does NOT cause nerve pain. Uncontrolled diabetes causes nerve pain and will
eventually damage the microvascular system, specifically the tiny blood vessels
in the extremities (legs usually), the eyes (the retina), and/or the kidneys.
These complications can lead to amputations, blindness and end-stage kidney
The mechanism is that when the blood
supply is cut off to the tiny blood vessels, they don’t supply the nerves with
the oxygen they need to receive and send signals; thus, you become insensitive
to pain or injury to your feet. A cut or some other undetected injury
of an uncontrolled diabetic
can thus lead to infection, then gangrene and amputation.
Uncontrolled diabetes is the culprit, NOT
diabetes. The point is that uncontrolled
diabetes – am I repeating myself? – is what needs to be avoided – and “treated”
when it’s encountered. The worst thing you can do is ignore a blood sugar
that is not in control. Over a period of years, it will
manifest itself. And you will likely die from it. And that’s scary.
Getting your blood sugar to the point
where it never exceeds
140mg/dl at any point after a meal and returns to under 100 mg/dl
(if you are pre-diabetic or a diagnosed Type 2) should be your goal. Any after-meal
spike above 140mg/dl are going to damage your microvascular system,
slowly but surely. And remember that an A1c of 7.0% (the ADA target!!!)
is equivalent to an estimated Average Glucose (eAG) of 154mg/dl. If you
have an average blood glucose of 154mg/dl (7%), just imagine how much of the
time your blood sugar is above 140mg/dl. Now, that’s, really scary.
So, how to you “treat” uncontrolled Type 2 diabetes?
Your doctor will probably start you on oral anti-diabetes meds and tell you to
lose weight, probably on a low-fat, “balanced” diet. You’ll probably also need
blood pressure meds, maybe a cocktail of them. Oh, and of course, a statin, to
lower your Total and LDL Cholesterol (because statins will do
that, although the benefit of doing so has not been shown). You should
know that under this regimen, your Type 2 diabetes will be a “progressive”
disease. That is, your condition will worsen; you will take more
and more medication, ultimately leading to injecting insulin. And don’t forget
the complications. They’re in your future too, including Macrovascular
complications (e.g., CVD). This is getting too scary even for me. But there is an alternative. Interested?
treat your Type 2 diabetes yourself. That’s right, YOU. YOU can control your blood glucose simply
by controlling the things you put in your mouth. The foods (and drinks) that
make blood sugar rise ALL contain carbs. Carbs, both the simple
sugars and the more complex carbohydrates (both processed and unprocessed),
when digested, all convert to glucose, or “sugar,” in your blood. The hormone
insulin transports and facilitates its uptake.
If you have T2 diabetes (or are
prediabetic), your body has over time become resistant to insulin, so the
glucose continues to circulate. In essence, you have become carbohydrate
intolerant. To control your diabetes, you only need to limit the amount
of carbohydrates you eat and drink. It’s that simple.
I’ve been writing about this subject
for 10 years. I’ve been a Type 2 diabetic for 33 years, the last 17 eating Very
Low Carb, (mostly) healthy foods. My Type 2 diabetes has not
progressed. In fact, it has been in remission for 17 years. I am
much, much healthier today that I was 17 years ago. You can be too, if YOU take charge of your diabetes
seated next to a Type 2 diabetic acquaintance at a church supper recently. As
the plates of food were passed around, I took a nice portion of ham and then (guiltily)
a serving of cole slaw. I knew it was loaded with added sugar, but I also knew
my other choices would be limited. I passed on the scalloped potatoes au gratin
and the peas, and the bread basket, and the sweetened ice tea, each time
passing the dish to my friend, who took a regular portion of each.
didn’t say anything, but I thought to myself, how can he do this to himself?
This man is somewhere in his eighties, skinny as a rail and looks healthy.
Maybe the question should have been, how does he get away with eating like
this? Eventually, I managed to open the subject with him. He responded by
saying, “I can eat whatever I want.” He then reached down to his belt and, out
of a small pouch, raised his pump controller to show me how he does it. My friend,
it turns out, is an insulin-dependent Type 2 with a pump that allows him to set
the amount of basal and mealtime (bolus) insulin before each meal. So, he knew
what was for supper – it’s the same every year – and had given himself a “shot”
via the needle imbedded under his skin. Voila! He can now “eat whatever he
wants” and “cover it” with insulin.
Type 2 diabetes with injected insulin has heretofore always been the last
resort of pharmacotherapy. Type 2s used to be started on a course of oral
pharmaceuticals and told to continue to eat a “balanced diet.” As one drug
failed to achieve the desired control (A1c’s within the ADA recommended range
the dose was increased and/or another class of oral introduced until the
patient, still eating “a balanced diet,” maxed out on three classes.
the dreaded insulin injection was employed for basal (slow acting for 24-hour
control) and mealtime “boluses.” Today, the introduction of new classes of
orals, and the (GLP)-1 receptor agonists, and more recently the new (SGLT)-2 inhibitor
drugs, that work on eliminating sugar in the blood via the kidneys, have
enabled some patients to delay multiple daily insulin injections. And “the insulin
pump” has replaced them all, for those who use it.
approach has been the introduction of injected insulin as a first course of
treatment. The rationale is that if you
eat a low carb diet, and inject a low dose of basal insulin once a day, you can
potentially achieve better control by reducing postprandial spikes (elevated
blood “sugars” after meals), thus achieving much lower A1c’s vs. the 7.0%.
Better control also means the surviving beta cells of the pancreas, that
produce endogenous insulin, get a rest.
of 7.0%, by the way, is equivalent to an estimated average glucose (eAG) of 154mg/dl, but an
A1c of 6.0% is an eAG of 126 and an A1c of 5.0% is an eAG of 97. This
improvement will surely reduce the possibility of the complications of poorly
controlled diabetes: retinopathy, neuropathy, and nephropathy (translation:
blindness, amputations and end-stage kidney disease). Plus, it reduces
the possibility of a much greater chance of a heart
attack. Any time your blood sugar
is above 140, you are causing damage, and an average of 154 means it is above
140 A LOT. It is, in my opinion, bordering on criminal to counsel
patients to only strive to achieve an A1c of 7.0%.
don’t write about insulin dependent Type 2s because I know very little about
it. Years ago, I read Richard K. Bernstein’s Diabetes Solution, the definitive source
book on the subject (for both Type 1s and Type 2s), but promptly forgot most of
the Type 1 details. His latest edition is very highly
regarded among those in the know. It is the “bible” for the growing numbers of T2s
as well as T1 diabetics who have discovered THE BEST WAY TO MANAGE AND CONTROL THEIR DISEASE IS TO EAT LOW CARB, with or without an insulin regimen.
because I rely on my dietary choices (plus a daily, single low-dose Metformin)
to directly limit the response
of my (broken) blood sugar metabolism, I’ll bet my blood sugar is more stable,
with fewer excursions, and therefore better controlled, than my friend’s (except
at this particular supper: LOL). I’d even venture to wager that my A1c is lower
than his. I didn’t ask him his, though. He, and his doctor apparently, are
happy with whatever it is, and he was very happy to be able to say, “I can eat
whatever I want.”
column was originally written in 2014. Sadly, my friend died of “complications”
(heart disease) in 2015.
The cognoscenti (my regular
readers, who are “in-the-know”) know that the answer is “high-fat.”
But I squirm in my seat when I hear someone, who appears to be informed on the
subject, say, “Low Carb is high-protein.”
That occurred one night in while I
was watching one of my favorite TV shows. The subject was a Wall Street Journal “Saturday Essay,”
titled, “The Questionable Link Between Saturated Fat and Heart Disease.” This
person accurately blamed the obesity epidemic on the American (or Western) diet
which is very high in carbs and processed foods; but then he proceeded instead
to advocate for a diet high in protein! That is WRONG, WRONG, WRONG!
Diets that are very high in
carbohydrates and processed foods ARE the reason we as a
civilization for 50 years have been getting fatter and sicker. The Wall
Street Journal got it right. They also correctly noted that the beginning
of this very large, population-wide, public health “experiment” in eating
“low-fat” can be attributed to Ancel Keys. I first wrote about Keys in
Retrospective #3, after Gary Taubes (Retrospective #5) brought him to my
Keys was an American physiologist
whose “Six Nation Study” (later revised to “Seven Country Study”) was just bad
science. This was just a few years after President Eisenhower had his heart
attacks and went on the Pritikin diet. Incredibly, however, low-fat quickly became
dietary dogma. Keys made the cover of Time Magazine in 1961 and joined the
American Heart Association board. It was later revealed that his studies were
Meantime, a low-carb
diet, which is the antidote to the fattening low-fat diet (you
read that right), is high fat and moderate protein.
Let’s talk numbers (percentages). Diets can be classified by what are called
The Low Fat Diet: The Standard American Diet
(SAD, for short!) is high carb, moderate fat and adequate but low protein. The
FDA’s Nutrition Facts Panel on processed foods, based on a 2,000 calorie a day
diet, is comprised of 60% carbs, 30% fat and 10% protein. The
dietary Dictocrats have recently recognized that simple sugars and processed
carbs are too high and have moved slightly away from the 60% carb percentage
(but not changed the package labeling). Still, they steadfastly maintained a
target of less than 30% fat. That can only
mean an increase in protein. To the extent carbs are reduced (from 60%) and
fats do not exceed 30% (while advocating a lower percentage), only protein can rise. Remember, there
are only three macronutrients: carbs, fat and protein. Something’s gotta go up!
In addition, a plant-based diet is
increasingly being advocated by the vegan lobby. All plants are carbohydrates.
Most protein (not all – there are some proteins in legumes and nuts) is
animal-based. So, the struggle to maintain a high-carb, low-protein macronutrient
ratio is an unrelenting battle within the establishment.
The Low Carb Diet: The macronutrient ratios for a
low-carb diet are not defined. They are all over the place. This is okay with
me since 1) people’s metabolic status (degree of carbohydrate intolerance) are
different and 2) making the transition from 60% carb to a much
lower percentage is a very good thing – but for some (who don’t go “cold
turkey” like me), it takes time and a lot of effort. So, let’s say for our
purposes that a prototypical Low Carb diet is 20% carb, 20%
protein and 60% fat. That’s a very dramatic (2/3rds) reduction in
carbs, from 60% to 20% (low), and a doubling of protein from 10% to 20%
(moderate) and fat, from 30% to 60% (high). That “high fat” is really scary for
some people, especially because there is disagreement (and therefore confusion
among the public) about what “good” fats are.
For that discussion, Google “the
nutrition debate good fats” for some of my columns on fat. But there is another
mitigating factor: All these percentages are in calories, and
since fat has more than twice as many calories per gram as both protein and
carbohydrates (9 vs. 4), you really are eating less than half as much fat (by weight) than you think.
Very Low Carb: I started “Low Carb” dieting at 20
grams a day, which is Very Low Carb: My first
ratios (as it turned out) were 10% carb, 30% protein and 60% fat. I later
tweaked that to 7% carb, 25% protein and 68% fat. Today, I aspire to eat 5%
carb, 20% protein and 75% fat (by calorie, remember, not weight).
Of course, we don’t eat percentages; we eat portions, which are envisioned in
the mind’s eye by mass (weight). These quantities and calorie percentages are
determined by software that some of the compulsive among us (including me) have
Low Carb is really moderate protein and high
fat. The lower the carb percentage, the higher the fat. Some call it, Low Carb High
Fat (LCHF). What does your Eating Plan
I’ve been writing this column since
2010. I started posting once a week, then twice, now, as Retrospectives, daily rewrites
at thenutritiondebate(dot)com. Some readers follow me by RSS feed, others on
Facebook and twitter, yet others by a link from other sites. Most readers,
however, are still introduced to “The Nutrition Debate” by Google searches on
topics of interest to them.
Blogger provides me with some simple
statistics or my readership by day, week, month and all-time. It also tracks my
audience by country, traffic source, and post (column), so I have a broad idea
of who, how and what my readership is.
Only 40% of my readers are in the U.
S. The Ukraine and Israel garner a little less than 10% each. Russia, France
and China come next, then Germany, Canada and the UK. Interestingly, Poland
rounds out the top ten. Once in a while I get 1,000 pageviews in a 1-hour period from Israel. Obviously,
someone who follow me there posts a link on their site.
I also have loyal followings in
Sweden, Hong Kong and Singapore. The Singapore readership in on a site where a
very popular and avuncular social network leader writes on the subject of
“Clean Eating.” He provides occasional links to my columns and has even posted
a few as permanent resources for his followers.
It’s interesting to me that I have so
many readers in Ukraine-Russia and China. I suppose that people there have
“hijacked” my content (with or without attribution, who knows?) and appear to read
everything I write. Some sites are commercial (e.g., department stores), others
are pornographic sites. All are in a Slavic language. I don’t object, mind you.
I write this column for educational purposes. There is no revenue, and I have
no interest in commercializing it.
This might also be a good time to
mention that I have a wonderful and intrepid volunteer editor, a person who
makes my writing clearer, checks my facts, and whose digital resources are
almost as vast as Google’s (slight exaggeration there). Her acumen in all
things health and nutrition is only exceeded by her generous heart and her
interest in spreading the word about good nutrition and healthy eating. I am
unabashedly in awe of her.
So, since Google seems to be the
main, continuing source of new readers, I encourage this method of using that
search engine. Just as Google has a “feeling lucky” search function, you could
do the same. Just type “The Nutrition Debate” (in quotes) in the “window,” (or,
thenutritiondebate(dot)com), hit “enter,” and let ‘er rip. I guarantee that my
blog will come up on the first page, or in the latter case, first.
Of course, if you want to do a more targeted search, you could do
something more “advanced.” Enter “The Nutrition Debate” and another word or
phrase of interest to you (or a column number, i.e., #xxx. Let Google do the
work! To see how well this works, I just entered “the nutrition debate
triglycerides” and all ten (10) Google
results were columns that I have written on triglycerides. This works
very well in the absence of “tags,” “labels,” or “key words.”
On the other hand, if you’d like to
see a list of all the columns I’ve written, in some browsers you
can see a list.“The Nutrition Debate List of Columns, appears at the top right
corner of the post, listed under “Favorite Links and Videos.” This works in
Chrome, but, alas, not in IE.
So, if you are one of those who rely
on Google (or another search engine), as I do, I encourage you to try this “advanced
search technique.” I am too much of a Luddite, or troglodyte, and too lazy at
this point, to go back over 500 columns and enter tags, labels and key words.
Use technology to search instead. It works for me. Just Google “the nutrition
debate” and another key word or phrase, and press “enter.”
Then, if you like what you have read,
go to the RSS feed and get my blog delivered every morning to your hand-held
device, tablet, laptop, or work station. And please, send me your comments and
ideas. I’m always looking for your feedback and subjects of interest to you, me
and my readers. It’s helps me get educated too.
In Retrospective #213 I told how, by just restricting carbs,
and later protein, that I ate for weight loss, my blood sugar control, blood
pressure, blood lipids, and inflammation markers all vastly improved. You (and your doctor) would be very happy to
have these results (as I and mine are), but the story doesn’t end there. There
is more to tell.
Starting at 375 pounds, I lost the first 60 pounds
in nine months (1½ pounds a week) by eating just 20g of carbs a day.
I wrote down everything I ate every day, estimating carb grams. No measuring – just
guessing. It gave me heightened awareness and accountability for what I decided
to eat – and I learned a lot about
which foods contained carbs and how they affected my blood sugar. When
I started Very Low Carb (VLC) in 2002, I had been a progressively worsening Type
2 diabetic for 16 years. I left my diabetes care to my doctor. Now, I rely on self-care for my
After 4 years, however, I began to slip and gained 12 pounds.
I wanted to lose those 12 pounds and a
lot more. That’s when I decided to count protein. I devised my own
method for determining how much protein to eat, which I explain in Retrospective
#213. I started at 90 grams of protein a day (1.1g/kg), later dropping in steps
to 60 grams (0.9g/kg).
That only left fat and total calories. I chose an online site
to do the calculations. All I had to do was to remember, truthfully, everything
I ate and enter the estimated amounts. The software did the rest.
I determined how many grams of fat to eat by backing into the
calculation. I wanted to lose 2 pounds a week. At 3,500 calories/pound that is
7,000kcal/wk., or 1,000kcal/day. If a mostly sedentary, older male who doesn’t
exercise needs 2,200kcal/day to maintain his weight, then I would need to eat
just 1,200 kcal/day to lose 2 pounds a week. And 90 grams of protein + 30 grams
of carbohydrate = 120 grams, times 4 calories/gram, equals 480 calories.
Subtracted from 1200, that leaves 720 calories for fat. At 9 calories/gram for
fat, that means my allowance for fat was 80 grams a day.
That’s where I started on Richard K Bernstein’s 6-12-12
program for diabetics. I didn’t care about macronutrient ratios or ketosis. I
just ate Very Low Carb and “moderate protein.” Result: I
lost 100 pounds in 50 weeks (2 pounds a week, as planned), lowering
my protein as I went along. I lowered protein from 90 grams to 75 and then
eventually, today, just 60 grams a day, which is 20% of 1,200kcal
and still 20% above
the USDA’s guidelines (50g/d or 10% of 2,000kcal).
Later, I became interested in Macronutrient ratios. The diet that worked for me (where
I lost 100 pounds) was 10% carbs (30g/day), 30% protein (90g/day) and 60% fat
(80g/day). Thirty percent protein is the highest percent most experts recommend
for protein, and then only if you have no kidney problems. Your blood markers
for kidney disease should be tested by your doctor before you start and
rechecked annually on any moderately high protein diet.
As I lost weight, and
discovered low carb foods that I liked for breakfast and lunch,
and ate good fats, and small low carb and protein
suppers, I lowered both my protein and carbs, and increased my fat percentages.
My macronutrient ratios changed, from 7% carb (20g), 25% (75g) protein and
68% fat (90g) to 5% carb (15g), 25% protein (75g) and 70% fat (90g).
Now, they are 5% carb (15g), 20% protein (60g) and 75% fat (98g). All of
these ratios are for 1,200kcal/day.
It’s pretty easy to eat this way because “my body” is telling
me that it is “happy.” I have come to think of my body as a separate entity
that I am living in. I just eat small meals at mealtimes. This is
called “non-homeostatic” eating. That is, I am not eating because
my body is telling me to; I am not hungry at mealtimes. I am
eating because breakfast, lunch and supper are “mealtimes.” My body decides
what to do with the food, to add fat or burn fat and maintain muscle.
So, what do I eat? Breakfast is 3 eggs, 1 strip
of bacon and a cup of coffee with heavy cream and a little stevia powder. Lunch
is usually a can of kippered herring snacks in brine or Brisling sardines (in
olive oil!). And supper is a small portion of protein, usually a fatty meat or
fish, and a low-carb vegetable, either tossed in butter or roasted in olive
oil. If I snack (before supper only), my favorite is celery with anchovy paste.
Sometimes I’ll have olives, or radishes with salt and a dollop of butter, or a
small portion of nuts. Macadamia nuts have the fewest Omega 6s, while
hazelnuts, almonds or pecans have moderate amounts. Cashews are too high in
carbs and walnuts much too
high in Omega 6s.
At my doctor’s suggestion, I started eating Very Low Carb
(VLC) in 2002 to lose weight. At the time I had been a long-term
(16yr) Type 2 diabetic. I have been very successful, at one point losing 188
pounds. I also had to give up most of my diabetes drugs while getting
“normal” fasting blood sugars (80s mg/dl) on only 1 low-dose Metformin
once a day.
When I began VLC 17 years ago, I was “maxed out” on two
classes of oral diabetes meds and starting a third. Within a day of
starting to eat just 20g of carbs a day, I got my first hypo (BG reading in the
50s). I ate a candy bar and called my doctor. Over the next few days he told me
to cut my diabetes meds three times, twice by half . As I lost
weight, my BP gradually dropped from 130/90 to 110/70 at the same meds. Over time
my HDL doubled and triglycerides dropped by two-thirds. My Hb A1cs are
now consistently in the mid-5 range, and both my HDL/TG ratio and my hsCRP,
an inflammation marker, are both usually under 1.0. I am never hungry. I have
lots of energy, and I feel great. By all these measures I am today (age 78) much healthier than I was 17
years ago. How did this happen? I’m going to tell you.
When I first started eating VLC, for a few years I wrote everything down that I ate but only counted estimated carbs.
I didn’t measure anything. I just listed everything I ate and guessed at the
carb content. I did this in an Excel table I created that totaled the estimated
carbohydrate grams daily. The math was simple and the method not very accurate, but I
was learning about low carb eating, and I was being totally
accountable and brutally honest. I was learning what foods raised my
blood sugar. This is a learning
process everyone eating Very Low Carb for blood sugar control must do.
Four years later I became interested in how much protein I
should eat. I decided to eat a similarly sized, small-to-medium portion of
protein with each meal, and to space the meals at regular intervals, ala
Richard K Bernstein, MD. Bernstein also counseled that, to lose weight you
reduce the portion size of protein for one meal, and if that wasn’t enough, a
second meal each day, due to its “insulin effect.” This would later guide
me to the low side on protein.
The “insulin effect” is about how half of every gram or ounce
of protein you eat is going to become glucose in your blood. This occurs after
the protein is digested into amino acids and, if not taken up by your muscles,
etc., is stored in the liver. There, through a process called gluconeogenesis,
it is converted to glucose when the body needs glucose. That is one of the main
mechanisms of Metformin: “to suppress the up-regulated synthesis of glucose by
the liver in the disregulated sugar-based metabolism that many people have
developed on a carbohydrate-based diet.” This glucose requires insulin for transport
and uptake. Elevated insulin in the blood stops weight loss: the
How much protein you should eat is dependent on several
factors: among them age, gender, and level of activity. If you are very
active, i.e. you exercise regularly, you will need more protein to repair and
maintain the muscle tissue you have developed and use. I don’t exercise at all
(except in my daily activities: gardening in New York and kayaking in Florida).
I don’t like to sweat, and besides, doesn’t exercise “work up an appetite”? If
you’re trying to lose weight, as I am, who wants to do that! So, I began a
search to find out how much protein the “experts” say I should eat.
The “experts” recommend a very wide range of
protein amounts, all based on “weight.” You need to pick one and go with it. The
one critical measure, though, is the “weight” that you use. It should
be your hypothetical “lean body weight.” The definition of “lean body weight”
is difficult to ascertain and frequently
misinterpreted and misguided. But lean body weight is
what you should use because protein is not required to maintain
your fat mass, or helpful in reducing it.
This latter point is particularly
true for the overweight, obese and morbidly obese, like me. For me (old, male, diabetic, morbidly
obese, relatively inactive and without excessive musculature to maintain), I
chose to define “lean body weight” as the middle weight of “normal” in the
WHO’s BMI chart for my height, now shrunken with age to 5’-10.”
The BMI table says that, at 5’-10”, my middle-of-normal
weight should be 150 pounds. In the beginning, though, I thought a “lean body
weight” of 150 pounds for me was ridiculous, so I substituted a
“goal” or “ideal” weight of 180
pounds. At 0.5g/lb. (1.1g/kg), that worked out to 90g of protein a day. Then,
after I had lost over 100 pounds, a “lean body weight” of 150 began to sound
realistic, so I reduced it to 0.4g/lb. (0.9g/kg), or 60 grams of protein a day.
you develop diabetes, your metabolism is deeply committed to converting as many
calories as it can into fat.”
We’ve all heard this sentiment expressed,
or felt this depressing thought, many times, but I was especially affected
recently when I read this quote on page 241 of Cate Shanahan’s Deep Nutrition. I urge you to read this
book, or at least my review in Retrospective #205 and her deeply
troubling observations about the medical “business” in #206.
Shanahan’s book has hundreds of
references, so I lament that the above quote is not sourced. I suppose it
should be understood as a summation of the totality of the material presented
in her book. In any case, the quote can be read as an expression of
exasperation that we, overweight and obese Type 2 diabetics, feel in our
unremitting efforts to lose weight. It does seem that everything we eat turns
to fat, and it is damnably difficult
to lose that fat.
As my readers know, I am always
interested (from self-interest as well as for educational purposes) in
understanding the mechanisms behind our complex metabolic environment, or milieu
intérior as the 19th century French physiologist, Claude
Bernard, described it. And I have gained some insights into why it is that
“everything I (ch)eat turns to fat” and why people with impaired glucose
tolerance (IGT) gain weight easily and lose weight with great difficulty.
In lay terms, IGT is the equivalent
of “carbohydrate intolerance,” described in Retrospective #84, “Carbohydrate
Intolerance – the new ‘buzz’ words.”” They are the outward manifestation of a
metabolic change called Insulin Resistance (IR), described in more detail in Retrospective
#99, “Natural History of Type 2 Diabetes.”
Bottom line: as our bodies transition
from a normal metabolism to a dysfunctional metabolism, very commonly
accompanied by weight gain as an
effect of this dysfunction, not
a cause, our bodies undergo several physiological changes. Laboratory
reports detail these changes. The most frequently tested are fasting glucose,
hemoglobin A1c (HgA1c), and the lipid panel (Total Cholesterol, LDL, HDL, and
TC/HDL ratio) and triglycerides. Sometimes, when these markers are “out of range,”
a diagnosis of Metabolic Syndrome is made. All too often, though, the doctor
prescribes a statin and tells the patient to “exercise and eat a low-fat diet”
to lose weight. There’s no pill for that prescription.
How have I come to this conclusion? Have
you had a similar experience? When I have been very good – that is, when I not
only talked-the-talk but walked-the-walk, every day – my fasting blood sugars are
consistently in the 80s. I can point to weeks, even months, of never or very
rarely having a Fasting Blood Glucose over 100mg/dl. And since it is an elevated
blood glucose that causes the pancreas to produce insulin, to
transport to and facilitate uptake of that blood glucose in their destination
cells, it is an elevated blood glucose level that causes
an elevated blood insulin level.
As my readers know, and as anyone who
has read Taubes’ Good Calories-Bad
Calories (The Diet Delusion in
the UK), or his more approachable Why We
Get Fat, elevated blood insulin CAUSES FAT STORAGE and PREVENTS FAT
BREAKDOWN for energy. Retrospective #5 presents Taubes’s “10
certain conclusions” from the GC-BC (pg. 453-454). It is a very succinct and
compelling explanation of the functional role of insulin in homeostasis, and a
Anyway, recently my fasting blood
glucose readings were in the 100 to 125 range. Obviously, while I have been
talking-the-talk, I have not always been walking-the-walk. I admit it. I “cheated”
a little almost every day; always just before or at any time
after dinner. And I pay the price. It was just a little “cheat,” so I didn’t
gain weight, BUT NEITHER DO I LOSE ANY WEIGHT, EVEN THOUGH
I AM EATING NO MORE THAN +/- 1200-1800 CALORIES MOST DAYS.
What’s happening is that my serum insulin levels are slightly elevated –
elevated just enough to turn everything I (ch)eat to fat and stop the
breakdown of body fat in storage even though I am eating below my
homeostatic level. My body “gets the message” that as long as I have a supply
of quick energy every night (the “cheats” that break down to glucose), it can
conserve my body fat, and lay on more with every calorie that isn’t needed to
maintain my basal metabolism while I sleep. The “signal” is: the slightly elevated
blood insulin circulating my slightly elevated blood glucose. If this is still
unclear to you, I urge you to read Retrospective #5 with Taubes’s “10 Certain