What About the Widely Advocated Dietary Restrictions on Fat, Protein, and Salt, and the Current High-Fiber Fad?
M o s t of this book is instructional, of the how-tovariety.
The intent of this appendix isto provide you with aUttle of the science that surrounds the program described in the restof the book.
With respect to anumber of the issues raised in this section, I would also refer you again to Gary Taubes's award-winning Science article "The Soft Science of Dietary Fat," which is avaUable on the Web site for this book, www.diabetes-book.com/articles/ssdf.shtml, or from the March 3,2001, edition of the journal Science.
Another mas terpiece by Taubes, "What If It's AU Been a Big Fat Lie?" appeared as the cover article in theNew York Times Magazine of July 2,2002.
It can also be found on this book's Web site.
I hope that I cancut through someof the myths that clouddiet and the treatment of diabetic complications sothatyou wiU have the why that supports the how-to.
We've already discussed someof the myths.
We'U lookatthe origins of those myths to try to give you as many of the facts as are avaUable at this writing.
If your only interest is in the how-to, feel free to skip this appendix.
Once you've started to foUow a restricted-carbohydrate diet, you may find yourselfpressured by weU-meaning but uninformed friends or famUy, or even newspaper articles, to cease penaUzing yourself and eat more"fun" foods — sweets, bread, pasta, and fruits.
This chapter wiU provide you with specific scientific information that underpins my approach and wiU perhaps give you some ammunition for re sponding to this pressure.
Even if you skip it now, you may want to come backto it later, or show it to your loved ones to lay their con cernsto rest.
As I don't expect most readers to be scientists, I've tried to keep aU these explanations relatively simple.
Some of the explana-
444 AppendixA
tions may at this moment represent more theory than fact, but they're based on the latest information avaUable to us.
HOW DID THE COMMONLY PRESCRIBED HIGH-CARBOHYDRATE DIET COME ABOUT?
If, like me, you've had diabetes for a whUe, you've probably been told to cut waydown on your dietary intake of fat, protein, and salt, and to eat lots of complexcarbohydrate.You mayeven still read this advice in publications circulatedto diabeticpatients.
Why is such advice being promulgated, when the major cause of such diabetic compUcations as heart disease, kidney disease, high blood pressure,and blindness is high blood sugar?
When I firstdeveloped diabetes, in 1946, Uttle wasknown about why this disease, even when treated, caused early death and such distressing compUcations.
Priorto the avaUabiUty of insulin, about twenty-five years earUer, peoplewith type 1 diabetes usuaUy died within a few months of diagnosis.
TheirUves couldbe prolonged somewhat with a diet that was verylowin carbohydrate and usuaUy highin fat.
Mostsufferers from the milder type 2 diabetessurvivedon this type of diet, without supplemen tal medication.
When I became diabetic, oral hypoglycemic agents were not avaUable, and many people werestiU foUowing very low carbo hydrate, high-fat diets.
It was at about this time that diets very high in saturated fats,with resultant high serum cholesterollevels, were experi- mentaUy shown to correlate with blood vessel and heart disease in ani mals.
It wasprompdyassumed bymanyphysicians that the then-known compUcations of diabetes, most of which related to abnormaUties of large or smattbloodvessels, were caused bythe high-fat diets.
I and many other diabetics were therefore treatedwith a high-carbohydrate, low-fat diet.
This new diet was adopted in the mid-1940s by the American Dia betes Association (ADA), the New York Heart Association, and eventu- aUy by the American HeartAssociation (AHA) and other groupsaround the world.
On the new diet, most of us had much higher serum choles teroland triglyceride levels, and still developed the grave long-termcom pUcations of diabetes.
Seemingly unaware of the importance of blood sugar control, the ADA raisedthe recommended carbohydrate content from 40 to 50 percent of calories, and then more recentiy to 60 percent.
The ADA's most recentguidelines havebackedoffbyvaguely stating that some diabetics may do betterwith less carbohydrate.
What About Dietary Restrictionson Fat, Protein, and Salt? 445
RECENT DEVELOPMENTS REGARDING RISK FACTORS FOR HEART DISEASE
In the past twenty years, researchstudies have generated considerable new information about heart disease and vascular (blood vessel) dis ease in general, and their relationship to diabetes in particular.
Some of this recent information is summarized here.
A number of substances have been found in the blood which relate to riskof heart attacks and vascular disease.
These includeHDL(high- density Upoprotein), LDL (low-density Upoprotein), triglyceride, fibrinogen, homocysteine, C-reactive protein, ferritin (iron), and Upo protein^).
High serum levels of dense, compact LDL particles, tri glyceride, fibrinogen, homocysteine, C-reactive protein, ferritin, and lipoprotein(a) tend to be associated with increasedcardiovascularrisk, whUe high levels of HDL tend to protect from cardiovasculardisease.
Cholesterol is a component of both LDL and HDLparticles.
The frac tion of total cholesterol found in LDL particles isan indexof risk,whUe the fraction of cholesterol found in HDL particles is an indexof pro tection.Nowadays, whenwewant to estimate the effects of Upids (fatty substances) upon the risk of coronaryartery disease, welook at the ra tio of total cholesterol to HDL and also at fasting triglyceride levels.
Someone with high serum HDL can thus have a high total cholesterol and yet be at lowstatistical risk for a heart attack.
Conversely, a person with lowtotal cholesterol and verylowHDLmaybe at high risk.
A large multicenter study (the LipidResearch ClinicsTrial) investi gatedthe effects of a low-fat, high-carbohydrate diet versus a high-fat, low-carbohydrate diet on nondiabeticmiddle-aged men with elevated cholesterol levels.
The study foUowed 1,900 people for seven years.
Throughout this period, total cholesterol had dropped only 5 percent from baseline in the low-fat group, but serum triglyceride went up about 10 percent! (Serum triglyceride rises very rapidly after a high- carbohydrate meal in nondiabetics, and moves up and down with blood sugarlevels in most diabetics.) As with prior studies, no signif icant correlation was found between serum cholesterol levels and mortality rates.
Furthermore, a study reported in the Journal of the American Medical Association in 1997 showed that a 20 percent in crease in either saturated or monounsaturated dietary fat loweredthe risk of stroke to one-eighth of what it was in individuals on lower-fat diets.
Unsaturated fats showed no such benefit.
On average, diabetics with chronicaUy high blood sugars have ele-
446 AppendixA
vated levels of LDL (the "bad" cholesterol) and depressed levels of HDL (the "good" cholesterol), even though the ADA low-fat diet has now been in use for many years.
Of great importanceis the recentdis coverythat the forms of LDLthat harm arteries are smaU, dense LDL, oxidized LDL, and glycated LDL.
AU of these increase as blood sugar increases.
In addition, independendy of blood sugars, high serum in sulin levelsdictatedby high-carbohydrate diets bring about increased production of the potentiaUy hazardous smaU, dense LDL particles and enlargement of the ceUs lining the arteries.
We now can measure the size distribution of these LDL subparticles as a routine laboratory test.
Most labs report the benevolent large, buoyant LDL subparticles as"type A." Under normal conditions, receptors in the liver remove LDL from the bloodstreamand signal the Uver to reduce its manufactureof LDL when serum levels rise even sUghdy.
Glucose may bind to the surface of the LDL particle and also to liver LDL receptors, so that LDL can not be recognized by its receptors.
In people with high blood sugars, many LDLparticles become glycosylated, and are therefore not cleared by the Uver.
This glycosylation is reversible if blood sugar drops.
After about 24 hours, however, a rearrangement of electronbonds occursin glycosylated proteins, so that the glucose can't be released even if blood sugar drops.
This irreversible glycosylation is caUed glycation, and the affected protein molecules are said to be "glycated." They are also referred to as AGEs, or advanced glycosylation end products.
These AGEs accumulate in the blood, where they can become incor poratedinto the waUs of arteries, forming fatty deposits caUed atherotic plaques.
Since Uver LDL production cannot be turned off by the glycosylated/glycated LDL (and also the presence of glycosylated/ glycated LDL receptors), the liver continues to manufacture more LDL,even though serum levels may be elevated.
The proteins in the waUs of arteries can also become glycosylated/ glycated, rendering them sticky.
Otherproteins in the bloodthen stick to the arterial waUs, causing further buUdup of plaque.
Serum proteins glycosylate in the presence of glucose.
White blood ceUs caUed macrophages ingest glycosylated/glycated proteinsand gly cosylated/glycated LDL.
The loaded macrophages sweU up, becoming very large.
These transformed macrophages, loaded with fatty mater ial, are catted foam ceUs.
The foam ceUs penetrate the now sticky arte rialwaUs, causing disruption of the orderly architecture of the artery, and narrowthe channel through which blood can flow.
What About Dietary Restrictions on Fat, Protein, and Salt? 447