Пишут что-то про исследования добавочного применения женьшеня при шизофрении: статья на CBS, запись в гос. каталоге клинических испытаний. В ПабМеде вроде ничего нет пока, так что относиться нужно со скепсисом..
Также некоторые исследователи предполагают, что у подгруппы больных могут смягчиться симптомы при добавлении витаминов, снижающих уровень гомоцистеина, в первую очередь фолиевой кислоты. Тут также нет однозначных доказательств, лишь косвенные зацепки: по некоторым данным, у больных, особенно у мужчин, повышен гомоцистеин (но высказывались сомнения в этих данных); высокий гомоцистеин вроде бы может вмешиваться в работу NMDA-рецепторов; с болезнью может быть связан ген MTHFR, участвующий в метаболизме фолата; при очень сильном повышении гомоцистеина (при редчайших мутациях) отмечаются психотические и депрессивные симптомы. Повторяю, пока не встречал результатов клинических исследований, говорящих, что довавление фолиевой кислоты - B9 ( а также B6, B12) влияет на симптомы. Но исследователи, работающие над глутаматной гипотезой, периодически эту тему поднимают. Вот, например, цитата из пресс-релиза вчерашнего публичного симпозиума NARSAD в Бостоне:
Folate as a Cause and Treatment for Schizophrenia: Who Will Benefit?
Do genes explain why some people with schizophrenia are helped when
they take supplements of the common B vitamin, folate? The answer is yes
and now, new NARSAD funded research is examining the reasons why.
According to Dr. Goff, whose pioneering research identified a link
between low blood levels of folate and negative schizophrenia symptoms,
folate is involved in many different chemical pathways in the brain,
including keeping levels of the amino acid homocysteine low. When
homocysteine levels are too high, this interferes with the functioning of
receptors located all over the brain – called NMDA ( N-methyl-D-aspartate)
receptors – that are critical to learning, memory, brain development, and
general neural processing.
However, what causes low folate in people with schizophrenia is still
open to question. One reason, confirmed by epidemiological studies, is poor
dietary intake. Based on examining two major famines in the 20th century –
the Dutch Hunger Winter of 1944-45 brought about by the Nazi occupation in
World War II and the Chinese famine in 1959-61 – scientists found that the
incidence of schizophrenia among children born to women who were pregnant
during these famines increased two-fold.
But in most cases, starvation is not the problem. That is why Dr.
Goff’s team looked for other causes, including two genes: GCPII (glutamate
carboxypeptidase II), which controls the absorption of folate and may be
deficient in people with schizophrenia, and MTHFR
(methylenetetrahydrofolate reductase), which activates folate for use in
the brain. Using this information, Dr. Goff and his colleagues are
recruiting patients for a large trial to determine whether folate
supplementation will help individuals affected by these genes, many of whom
have treatment-resistant psychotic symptoms. Funded by the National
Institute of Mental Health, this double-blind study will follow 150
patients with schizophrenia at three sites over a 16-week period.
“Schizophrenia is a prevalent and costly disorder and can be very
difficult to treat. This is especially true for the estimated 30 percent of
patients with treatment-resistant psychotic symptoms, who may also
experience social withdrawal, apathy, and depression,” reports Dr. Goff.
“Having these new data will validate whether folate, which is known to be
very safe, is an effective way to improve outcomes for people with
schizophrenia who now suffer from treatment-resistant psychotic symptoms.
Building on this landmark research, scientist and colleague, Joshua
Roffman, MD, is using NARSAD funds to go the next step – identifying
people with schizophrenia who are most likely to benefit from folate
supplementation. Here, Dr. Roffman and his colleagues started with the
MTHFR gene and found that one variant increases the severity of
schizophrenia symptoms. Moreover, in patients with this variant, low folate
intake was associated with symptoms that were especially severe.
Now, Dr. Roffman’s team is looking at the combination of MTHFR and
another gene – COMT (catechol-O-methyltransferase) – that affects
dopamine levels in the brain. Although the two genes have separately been
associated with schizophrenia, Dr. Roffman’s just completed study finds
that when these genes interact, a specific subset of patients is at greater
risk for cognitive impairment. In individuals who carry the risk variants
of both MTHFR and COMT, lower-than-normal levels of dopamine in the part of
the brain called the prefrontal cortex may cause problems with information
processing and working memory. Using functional neuroimaging, Dr. Roffman
and his colleagues also found that the same combination of MTHFR and COMT
variants were associated with abnormally low activity in the prefrontal
cortex.
“We now have the techniques to determine how genes combine to produce
schizophrenia symptoms,” Dr. Roff explains. “As we gain a better
understanding of individual biogenetic pathways, we can identify high-risk
groups and those most likely to benefit from specific treatments.”
Возможно, они попытаются подобрать группу пациентов с неудачными вариантами генов MTHFR, GCPII, (а также сочетанием MTHFR-COMT и низким фолатом в крови?) и провести исследование. Тогда посмотрим, правы ли Goff и его единомышленники.
