I would really hate to have to read the whole book but I might have to if enough doctors ask me specific questions about it. In the absence of any specific questions I will just say that since Dr. Wolcott consulted me repeatedly throughout the time he was writing it I am intimately familiar with its overall theme if not with its specific contents.

Dr. Wolcott is one of the few people in this business who understands the concept of metabolic typing -- so for that reason everything he says is worth hearing. However, everything that is in Wolcott’s system that is of value is already included in Nutri-Spec. The rest of what is in Wolcott’s system is probably not inaccurate enough to do anyone any real harm – but it requires a doctor or patient to invest a tremendous amount of time, energy and money in things that simply are not clinically significant.

What Wolcott and Kristal call “fast and slow oxidizers Nutri-Spec knows as GLUCOGENIC and KETOGENIC. (We have explained several times over the years in NUTRI-SPEC LETTERS, etc. why “fast and slow oxidizers” is a misnomer, totally misses the essence of the imbalance, and is misleading to Doctors and their patients who try to work with these confusing terms. Þ GLUCOGENIC and KETOGENIC imbalances have nothing to do with the rate of oxidation. (These terms were originally used by the hair analysis people who totally misinterpreted Watson’s work which they “borrowed.”) What is fast and slow about GLUCOGENIC and KETOGENIC patients is the rate at which they clear glucose from the serum.)

Regarding Wolcott’s Oxidative Type model: The picture will be more clear if you think of GLUCOGENIC patients not as excess oxidizers of carbohydrate (since many of them do not oxidize excess carbohydrate – they convert it to body fat), but as deficient oxidizers of fat. Similarly, think of KETOGENIC patients as deficient oxidizers of carbohydrate, not excessive oxidizers of fat.

KETOGENIC ENERGY FORMATION Þ KETOGENIC patients must rely too much on beta oxidation since they do not easily metabolize carbohydrates. This process produces only 70% as much CO2 as carbohydrate metabolism, which explains the ALKALINITY of your KETOGENIC patients.

GLUCOGENIC patients are the opposite. Þ They cannot easily metabolize fats, so they depend too much on glycolysis and the Krebs cycle. This is why they produce more CO2 in proportion to their total quantity of oxidative metabolism (but low CO2 in absolute terms).

The NUTRI-SPEC FUNDAMENTAL DIET (NSFD) is the foundation upon which you build each patient’s individualized eating plan. If that patient is GLUCOGENIC or KETOGENIC you integrate the specific GLUCOGENIC/KETOGENIC diet recommendations with the NSFD. So – GLUCOGENIC gets a lower than average carbohydrate:protein ratio; KETOGENIC gets a higher ratio. GLUCOGENIC must minimize the tomatoes, onions, etc; KETOGENIC must emphasize the white poultry and fish, and eggs, etc., etc. These dietary specifics do directly impact the decreased serum pH of GLUCOGENIC and increased serum pH of KETOGENIC.

The notion that SYMPATHETIC and PARASYMPATHETIC patients are characterized by acid and alkaline serum pH is an error. It is an error that Wolcott “learned” from his mentor and former employer Kelley (of the infamous “Kelley Programs”). Kelley’s mistake was that he misinterpreted the writings of Pottenger on the autonomic nervous system – thus mistakenly concluding that Pottenger’s SYMPATHETIC and PARASYMPATHETIC were identical to Watson’s KETOGENIC and GLUCOGENIC. When Wolcott began to work independently, he realized that Kelley had been wrong, recognized that KETOGENIC & GLUCOGNEIC and SYMPATHETIC & PARASYMPATHETIC were different, but held on to Kelley’s belief that PARASYMPATHETIC and SYMPATHETIC are associated with serum pH aberrations.