If It’s Becoming More Common, It’s Not Genetic!

Don’t get me wrong. I think that the Human Genome Project was a great idea. How­ev­er, I don’t think that genet­ic stud­ies are going to help us unrav­el our main caus­es of death and dis­abil­i­ty in the Unit­ed States. That’s because they are large­ly the result of our food, not our genes. You can tell this from the sim­ple fact that the rates of these dis­eases go up and down, depend­ing on how a pop­u­la­tion eats.

The rate of tru­ly genet­ic dis­eases (such as hemo­phil­ia or cys­tic fibro­sis) stays remark­ably sta­ble in a pop­u­la­tion from one gen­er­a­tion to the next. The only way it could increase is if there were a sud­den wave of immi­gra­tion of peo­ple car­ry­ing the gene (in which case, the dis­ease would most­ly be in the immi­grants and their chil­dren) or if the peo­ple with the gene sud­den­ly became much more fer­tile (which is unlike­ly).

When you see the rate of a dis­ease go up and down dra­mat­i­cal­ly with­in the space of 10 years, you know for sure that the cause of that change is envi­ron­men­tal, not genet­ic. The clas­sic illus­tra­tion is the sharp decline in heart dis­ease in Nor­way dur­ing World War II. After the Nazis invad­ed Nor­way (and stole a lot of their farm ani­mals), the Nor­we­gian pop­u­la­tion had to shift to a low-fat, plant-based diet. As a result, the dis­eases of afflu­ence (heart dis­ease, type 2 dia­betes, mul­ti­ple scle­ro­sis) became much less com­mon. The rates of those dis­eases went right back up again after the war end­ed and peo­ple went back to their old ways of eat­ing.

Anoth­er clue to whether a dis­ease is genet­ic or envi­ron­men­tal comes from its geo­graph­ic dis­tri­b­u­tion. If a dis­ease is most com­mon in an area with small gene pool, it’s like­ly to be genet­ic. Exam­ples include the hered­i­tary deaf­ness that was once com­mon on Martha’s Vine­yard and Tay-Sachs dis­ease in East­ern Euro­pean Jews and French Cana­di­ans. These are reces­sive gene dis­eases. You can get the dis­ease only if you got the same defec­tive gene from both par­ents, which is most like­ly to hap­pen if they are relat­ed to each oth­er.

On the oth­er hand, if a dis­ease is most com­mon in an area whose pop­u­la­tion came from a wide vari­ety of immi­grants, then you can bet your bot­tom dol­lar that the under­ly­ing cause for the high rate of the dis­ease is envi­ron­men­tal, not genet­ic. The clas­sic exam­ple of this is Parkin­son dis­ease, which is most com­mon in Buenos Aires, Argenti­na. Although there may be some genes that pre­dis­pose a per­son to Parkin­son dis­ease, espe­cial­ly the ear­ly-onset form, the fact that the world’s high­est rate is in a pop­u­la­tion made up of recent immi­gra­tion from many dif­fer­ent places tells me that the major risk fac­tor is some­thing in the envi­ron­ment. Con­sid­er­ing that the peo­ple of Buenos Aires also eat more beef than any­one else in the world, I’d be will­ing to bet that the envi­ron­men­tal fac­tor is red meat con­sump­tion.

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Red Meat, Vitamin B2 Deficiency, and Parkinson Disease

Recent­ly, some­one in my fam­i­ly got a diag­no­sis of Parkin­son dis­ease, which is the same dis­ease that Michael J. Fox has. So nat­u­ral­ly I searched the med­ical lit­er­a­ture to see if there was a dietary angle to the dis­ease. There is, and it’s very excit­ing! Remov­ing red meat from the diet and cor­rect­ing a vit­a­min B2 defi­cien­cy might pre­vent Parkin­son dis­ease, and it might even help reverse some of the effects of the dis­ease. This would actu­al­ly change the course of the dis­ease, where­as all doc­tors can do at present is treat its symp­toms.

How I Searched the Medical Literature

I went to http://www.pubmed.com/ and clicked on MeSH Data­base. Then I typed Parkin­son dis­ease in the search box and clicked on Go. One of the results was Parkin­son dis­ease. I clicked on that and select­ed the sub­head­ing “diet ther­a­py” and added that to the search box. Then I clicked on Search PubMed.

What I Found

One of the arti­cles that I found point­ed out that Parkin­son dis­ease is far more com­mon in elder­ly peo­ple in Europe and North Amer­i­ca than it is in elder­ly sub-Saha­ran Black African, rur­al Chi­nese, and Japan­ese peo­ple. In oth­er words, it’s far more com­mon in peo­ple who eat a lot of meat than in peo­ple who eat a heav­i­ly plant-based diet.

Anoth­er inter­est­ing arti­cle sug­gest­ed that Parkin­son dis­ease might result from two sep­a­rate prob­lems relat­ed to diet and nutri­tion (High dos­es of riboflavin and the elim­i­na­tion of dietary red meat pro­mote the recov­ery of some motor func­tions in Parkinson’s dis­ease patients. C.G. Coim­bra and V.B.C. Jun­queira. Brazil­ian Jour­nal of Med­ical and Bio­log­i­cal Research, 36: 1409–1417, 2003). The first prob­lem is an over­load of iron from eat­ing too much red meat. The sec­ond is some prob­lem in the way the body han­dles riboflavin (vit­a­min B2). To put these ideas to the test, the researchers test­ed 31 con­sec­u­tive Parkin­son dis­ease patients who entered their clin­ic. Every sin­gle one of them had abnor­mal­ly low lev­els of vit­a­min B2 in their blood­stream, even though they were eat­ing food that should have pro­vid­ed enough vit­a­min B2. In com­par­i­son, only 3 out of 10 patients with oth­er neu­rode­gen­er­a­tive dis­eases had a vit­a­min B2 defi­cien­cy. The Parkin­son patients were also big red meat eaters. The researchers told the Parkin­son dis­ease patients to stop eat­ing red meat and to take 30 mg of riboflavin three times a day.

The patients who fol­lowed this advice regained some of their lost motor skills. Mild­ly afflict­ed patients became com­plete­ly asymp­to­matic, and even some of the more severe­ly afflict­ed patients improved a lot. These find­ings were dra­mat­ic and excit­ing, and this arti­cle should have lit a fire under the researchers who are study­ing Parkin­son dis­ease. Here was a sim­ple, cheap, and safe dietary mod­i­fi­ca­tion that addressed the actu­al cause of the dis­ease, and could even reverse some of its effects.

Unfor­tu­nate­ly, peo­ple tend to dis­card the results of dietary stud­ies out of hand, part­ly because these stud­ies can’t fol­low the same for­mat as a drug tri­al. For exam­ple, you can’t “blind” peo­ple to what they’re eat­ing, so there’s nev­er a “place­bo con­trol.” Also, some peo­ple become total­ly unhinged if they hear that the foods they like aren’t good for them. Pre­dictably, some­one wrote in a tru­ly idi­ot­ic cri­tique of the study (Com­ments of H.B. Fer­raz et al. ) The authors’ response was with­er­ing. They said things like “By search­ing the cur­rent med­ical lit­er­a­ture, Fer­raz and asso­ciates might read­i­ly become famil­iar with count­less pre­lim­i­nary stud­ies which have been sub­se­quent­ly con­firmed by larg­er and bet­ter con­trolled research” and “The cita­tions made by Fer­raz and asso­ciates demon­strate that they have com­plete­ly missed our point, even though it was clear­ly empha­sized even in the title of our study.” What a smack-down!

Fer­raz and cowork­ers were wor­ried that if peo­ple stopped eat­ing red meat, they might end up with a pro­tein defi­cien­cy. Well, where do goril­las get their pro­tein? If a diet with­out red meat pro­vides enough pro­tein for a 500-pound sil­ver­back male goril­la, it should pro­vide enough for a human being. And what would be the harm in test­ing Parkin­son dis­ease patients for riboflavin defi­cien­cy? Why aren’t Fer­raz and cowork­ers wor­ried about the pos­si­bil­i­ty that we’re miss­ing an oppor­tu­ni­ty to stop Parkin­son dis­ease in its tracks?