Recently there was anarticlewhich raised some red flags for me. It explains why we can't be jumping to all sorts of conclusions about genes and their effects. From Medical News Today:
"UMaine psychology professors Merrill F. "Pete" Elias, Michael A. Robbins and Penelope K. Elias, in collaboration with colleagues in Syracuse, N.Y., England and Australia,studiedthe relationships among the gene ApoE, homocysteine concentrations, and cognitive performance" This prompts me to ask what variants did they study and what do they mean by cognitive performance?
Nine hundred eleven dementia-free and stroke-free subjects (59% women) from the Maine-Syracuse study (26–98 years old) were stratified into no-ApoE-4 (n = 667) and ApoE-4 carrier (n = 244) cohorts
The clinical diagnosis of dementia was determined from cognitive data, self-report, and medical records, using the National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer’s Disease and Related Disorders Association (NINCDS-ADRDA) criteria This is quite a few people, but they do not eliminate those patients who may have had a TIA or separated them by IQ. Which is probably a better way to assess this. In addition, Self report is a notoriously poor way for dementia patients to identify themselves. Remember these people who have dementia frequently deny that they have dementia.
Participants completed the Center for Epidemiological Studies Depression Scale (CES-D [34]) within one week prior to neuropsychological testing. Following a fast from midnight, a blood sample was drawn and a light breakfast was served. A physical examination and neuropsychological testing followed. Probably some of the best testing so far.... What did they find?
With adjustment for the Expanded model (Basic +CVD+ B-vitamin covariates), we found that persons with high, as versus low, plasma tHcy in the presence of an ApoE-4 allele performed 0.30S.D. and 0.40S.D. lower on the Global composite and the MMSE, respectively. Deficits of this magnitude are of considerable importance at the population level and constitute a risk factor for dementia Here's where the researchers make a huge error! They state "But there is hope for prevention and reversal of cognitive deficit related to elevated homocysteine by reducing homocysteine levels." Great! If you have Apo-E4 you should take folate? No! Hope? Listen, thissame old storywas thought to be true for cardiovascular disease. "We'll give you folate to lower your risk for heart attack" What happened?Nothing. In fact recently there is literature hinting that folate may actuallyincrease your riskof colon cancer growth!
The Sherpa Says: So where does this leave us? Is Folate good for those with APO-E4? Don't starting taking it yet. Nutrigenomics is coming, but the data, much like in Personalized Genomic testing, is not there yet. In Folate's case, what you don't know might actually kill you. Or At least give you colon cancer. That's why you need the Sherpas, to guide you through the study trail!
From Medical News Today:
"UMaine psychology professors Merrill F. "Pete" Elias, Michael A. Robbins and Penelope K. Elias, in collaboration with colleagues in Syracuse, N.Y., England and Australia,studiedthe relationships among the gene ApoE, homocysteine concentrations, and cognitive performance"
This prompts me to ask what variants did they study and what do they mean by cognitive performance?
Nine hundred eleven dementia-free and stroke-free subjects (59% women) from the Maine-Syracuse study (26–98 years old) were stratified into no-ApoE-4 (n = 667) and ApoE-4 carrier (n = 244) cohorts
The clinical diagnosis of dementia was determined from cognitive data, self-report, and medical records, using the National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer’s Disease and Related Disorders Association (NINCDS-ADRDA) criteria
This is quite a few people, but they do not eliminate those patients who may have had a TIA or separated them by IQ. Which is probably a better way to assess this. In addition, Self report is a notoriously poor way for dementia patients to identify themselves. Remember these people who have dementia frequently deny that they have dementia.
Participants completed the Center for Epidemiological Studies Depression Scale (CES-D [34]) within one week prior to neuropsychological testing. Following a fast from midnight, a blood sample was drawn and a light breakfast was served. A physical examination and neuropsychological testing followed.
Probably some of the best testing so far....
What did they find?
With adjustment for the Expanded model (Basic +CVD+ B-vitamin covariates), we found that persons with high, as versus low, plasma tHcy in the presence of an ApoE-4 allele performed 0.30S.D. and 0.40S.D. lower on the Global composite and the MMSE, respectively. Deficits of this magnitude are of considerable importance at the population level and constitute a risk factor for dementia
Here's where the researchers make a huge error! They state "But there is hope for prevention and reversal of cognitive deficit related to elevated homocysteine by reducing homocysteine levels."
Great! If you have Apo-E4 you should take folate? No!
Hope? Listen, thissame old storywas thought to be true for cardiovascular disease. "We'll give you folate to lower your risk for heart attack" What happened?Nothing. In fact recently there is literature hinting that folate may actuallyincrease your riskof colon cancer growth!
The Sherpa Says:
So where does this leave us? Is Folate good for those with APO-E4? Don't starting taking it yet. Nutrigenomics is coming, but the data, much like in Personalized Genomic testing, is not there yet. In Folate's case, what you don't know might actually kill you. Or At least give you colon cancer. That's why you need the Sherpas, to guide you through the study trail!