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Authors: Charles Spender

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Based on my experience with different types of raw food, I can draw the following conclusions. Judging by mental state or mental performance, there is no discernible difference between raw fruits/vegetables and cooked fruits/vegetables, if they are cooked at moderate temperature. There is no discernible difference between raw milk and pasteurized milk.

There is a significant difference between raw meat and fish and cooked meat and fish. Taking beef as an example, raw ground beef (15% fat or higher) typically has the following effects. These effects can manifest themselves within 30-60 minutes after a meal that consists of 300-500 grams (0.7 to 1.1 lbs.) of beef only: improved mood, reduced fatigue, increased self-esteem, increased capacity for work, improved attention control and impulse control. In contrast, an identical meal that consists of cooked beef will have the following effects: apathy and lowered mood, slightly increased fatigue, increased self-esteem, increased capacity for work, improved attention control and impulse control. Cooked animal products tend to lower mood and increase fatigue, whereas raw animal products have the opposite effects. Nonetheless, an ancestral diet that contains large amounts of uncooked red meat (1-2 pounds a day) may slightly increase physical fatigue after several months. Both cooked and raw meat increase capacity for work and improve attention and impulse control, although cooked meat seems to be more beneficial for self-control than raw meat (we are talking about forcing oneself to do necessary things and preventing oneself from doing unwise things). Cooked meat can cause
constipation
or hard stool if a person eats a large amount in one sitting; this is not the case with raw ground meat. Nevertheless, the combination of large amounts of raw ground meat (1-2 pounds a day) and large amounts of milk (2-3 liters per day)
may
cause constipation.

There is also a noticeable difference between raw grains and cooked grains with respect to effects on mental state, as you saw in the main text.

After a long and healthy hiatus, I tested the ancestral diet recently, when I became severely depressed in late April–early May 2011 (according to the diagnostic criteria in DSM-IV-TR [
340
], except the duration was less than two weeks), and the antidepressant diet was somewhat helpful, but not effective. This prompted me to try the ancestral diet. (
Warning:
Before you read any further, please review the cautionary information in Tables
1
and
7
.
) The ancestral diet consisted of raw ground beef, raw ground chicken (about a pound (0.5 kg) of meat per day total), raw eggs (washed with soap, 3-5 per day), raw and boiled fruits and vegetables and one to two glasses of pasteurized milk per day. The diet excluded cooked grains, legumes, artificial chemicals, seasonings, and so on. At the end of the first day of this diet, May 6, I came down with some sort of food poisoning, probably from the pathogenic bacteria in the frozen raw ground beef that I bought at a small local grocery store. This meat tasted funny and I threw it out right away and instead bought freshly ground raw beef and chicken at a nearby supermarket. As a precautionary measure, I did not eat any raw animal products on May 7 and 8, when I was ill with the food-borne disease (did not follow any special diets during this time). I presented with nausea, stomachache, general weakness, fever, and diarrhea. I treated these symptoms with adapted cold showers (three times a day), acetaminophen, phthalylsulfathiazol, and complete colon cleansing (one session) as described
at the end
of endnote B. All symptoms of the infectious disease were gone on May 9, when I decided to resume the ancestral diet using raw meat that I thought was from the safest source. My depressive symptoms improved somewhat on May 6, in spite of the infectious disease. I felt a relief of symptoms of depression on the second consecutive day of the ancestral diet (May 10), and I was completely cured of depression on the fourth day of the diet (May 12). I discontinued the ancestral diet on May 13. There were no food-borne infections during the second trial of the ancestral diet (May 9 through May 13); the diet was interrupted briefly on May 11 with a large meal (all kinds of food) and alcohol at a social event at work. I also used hydrotherapy during this depressive episode: an adapted cold shower in the morning and a head-out hot shower at night (I did not use hot showers during a fever).

 

 

Endnote E
(for biomedical researchers)

 

(L
AY
L
ANGUAGE
S
UMMARY
): The liver contains a great number of enzymes responsible for neutralizing various unusual compounds such as toxins and mutagens. This collection of enzymes is called the “liver detoxification system,” or “P450 system.” It is possible that when the diet changes, some of these enzymes become more active, while others become less active because now they have to deal with a changed set of chemicals. This change in the pattern of activity of the liver detoxification system can cause changes in how mutagens from cooked meat are neutralized by this system.

 

This is because under the changed conditions, each liver enzyme has to deal with a different load of chemicals compared to the normal metabolic state (or compared to the regular diet), and occupancy of each type of enzyme changes. This change in the pattern of activity of the liver detoxification system can cause changes in how this system neutralizes mutagens from cooked meat. Therefore, it is possible that during the normal metabolic state (carbohydrates serve as the main fuel), the liver does not neutralize cooking mutagens completely, and they have negative effects on mood. It is possible that during ketosis the liver neutralizes the mutagens from cooked meat more effectively, and the dieter does not feel any negative changes in mood. Similarly, changes in the activity of the liver detoxification system may occur when the diet includes large amounts of low-fat milk.

 

 

Endnote F
(for biomedical researchers)

 

Theoretical evidence of neuroleptic effects of a temporary protein-free diet
(L
AY
L
ANGUAGE
S
UMMARY
): The use of radical dietary changes for the treatment of brain disorders is not a new idea; for example, a ketogenic (high-fat, low-carbohydrate) diet is beneficial for treatment-resistant epilepsy [
451
,
578
] and a restrictive elimination diet can be effective in attention deficit hyperactivity disorder [
67
]. It is possible that a temporary very-low-protein, low-fat diet may have antipsychotic properties because this diet will cause some changes in the brain that are similar to those of antipsychotic (a.k.a. neuroleptic) drugs. These changes include a reduction in the level of a chemical called dopamine in the relevant brain regions and the changes in certain receptors for dopamine. Low-protein diets also produce some changes in the behavior of laboratory rats that are similar to those caused by antipsychotic drugs.

 

It is possible that a temporary very-low-protein, low-fat diet may have an antipsychotic effect because this diet will have some neurobiological effects that are similar to those of neuroleptic drugs.

 

  1. One study on experimental animals has shown that a low-protein diet reduces the density of dopamine D2 receptors in the striatum [
    579
    ] and also reduces the total level of dopamine (extracellular and intracellular) in this brain region and in the ventral tegmental area [
    329
    ]. The reduced density of D2 receptors was not accompanied by a change in receptor sensitivity. Reduction of dietary protein can reduce the level of a major metabolite of dopamine, homovanillic acid, in cerebrospinal fluid of humans, which is suggestive of reduced dopaminergic activity in the brain [
    580
    ]. A low-protein diet worsens coping behavior in the Porsolt swim test, which is an animal model of depression [
    466
    ]. These changes are consistent with reduced dopaminergic activity in the brain and are similar to the effects of neuroleptic drugs. Neuroleptics typically inhibit activity of most dopamine receptors (D1, D2, D3, and D4) but their antipsychotic effect is attributed to their antagonism of dopamine D2 receptor in the brain. Neuroleptics also worsen coping behavior (promote behavioral despair) in the animal models of depression [
    448
    ]. In humans, neuroleptics lower mood within hours [
    460
    ,
    461
    ]. There is one caveat with the above argument, in that neuroleptics cause a compensatory increase in the density of dopamine D2 receptors [
    581
    ,
    582
    ], and they cause an increase of extracellular dopamine in the brain due to inhibition of presynaptic D2 receptors [
    583
    ,
    584
    ]. Nonetheless, overall, neuroleptics tend to downregulate dopamine activity in the brain due to inhibition of postsynaptic dopamine receptors [
    585
    ].
  2. Dietary fat manipulations in laboratory animals affect the density of D2 receptors as well as the density of the dopamine transporter in the striatum [
    586
    ,
    587
    ]. This suggests that a low-fat diet may change the activity of the dopamine system in the brain.
  3. Additionally, reduction of dietary protein reduces the synthesis and turnover of serotonin in the brain of primates [
    588
    ] (the opposite is true in rodents [
    589
    ]). The attenuation of cerebral dopaminergic and serotonergic transmission by a low-protein diet may mimic some effects of clozapine, which has an inhibitory effect on several serotonin receptors (5-HT
    2A
    , 5-HT
    2C
    , and possibly 5-HT
    3
    and 5-HT
    6
    [
    590
    -
    595
    ]) and dopamine receptors (D1, D3, and D4) in addition to its relatively weak D2 receptor blockade [
    594
    ,
    596
    -
    599
    ].
  4. Some authors have reported that low-protein diets increase the plasma and brain level of glycine without affecting those of glutamate [
    305
    ,
    600
    -
    602
    ]. This may enhance the function of n-methyl-d-aspartate (NMDA) receptors and have a beneficial effect on negative symptoms of schizophrenia according to the NMDA hypofunction hypothesis of schizophrenia [
    603
    ].
  5. High-carbohydrate diets (low in fat and protein) are not uncommon among mammals, as there are a number of species that are frugivores, although the closest genetic relatives of humans among primates are omnivores [
    44
    ,
    45
    ].
  6. The fruit-and-vegetable diet (
    fifth section
    of Chapter Three and
    Appendix II
    ) can be considered an ancestral diet of primates [
    44
    ,
    45
    ] and it contains tiny amounts of protein and fat. The quality of protein is also low in this diet because of its plant origin [
    120
    ,
    318
    ,
    319
    ]. For this reason, the fruit-and-vegetable diet is basically a “protein-free diet.” As explained in
    Chapter Three
    , this diet may serve as an experimental model of ADHD and my personal experience suggests that it increases distractibility within one day and can cause a loss of interest in many activities if a person stays on the diet for 4 days or longer. These effects are consistent with hypofunction of the dopaminergic system in the brain [
    580
    ,
    604
    ], and therefore, the fruit-and-vegetable diet may have a neuroleptic effect. Initially, this diet seems to increase the activity level, but it returns to the normal level after about 4 days. In other words, this diet does not have sedative properties.

 

Readers can find a more detailed discussion of this topic elsewhere [
577
]. I have tested the fruit-and-vegetable diet extensively on myself, but since I have never had a diagnosis of a psychotic disorder, it is unknown if this approach can be effective as a neuroleptic treatment. In principle, the dietary and pharmacological approaches are not mutually exclusive and can be combined if necessary. The grains-only diet (
Appendix II
) contains low amounts of protein and the quality of protein is low too [
120
,
318
,
319
,
835
,
836
,
853
,
912
]; it may serve as a
sedating
neuroleptic treatment.
Endnote N
describes another approach to nonpharmacological inhibition of cerebral dopaminergic activity. Generally speaking, any radical dietary changes are a slow, non-invasive form of shock therapy for the brain and therefore may benefit schizophrenic patients. Electroconvulsive therapy is beneficial in psychosis [
936
] and the same is true for insulin shock therapy. There is a case report of a complete cure of schizophrenia after switching to a ketogenic diet [
870
].

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