If you should choose to drink alcohol -- which is best?

[CoachDD]

I think there is so much more to this - particularly with folks who have MTHFR mutations. Personally, I began having difficulty with sulfites and found that on the very limited occasions where I choose to drink, I can only tolerate gluten-free ciders.

[Julie G]

A few months ago I read a review article on alcohol risks and Alzheimer's. I was particularly interested in studies that teased out differences, if any, related to genetics. I found it interesting that there were many research articles that indicated no increased risk of AD with light to moderate alcohol consumption, even in APOE4+. I chased down some of the cited studies for further reading to find out if those participants were just too young to have AD, or if they were tremendously fit, or if moderate drinking actually meant "rarely", or if they all lived on the island of Ikaria - but could see nothing that would indicate why in certain (many) studies, no increased risk was observed

FF, can you share some of these studies with us. I find the opposite when I review the literature .

[McGido]

Get these things right consistently:

- Getting ample quality sleep
- Healthy exercise routine
- Frequent contact with nature
- Consistently challenging yourself cognitively (learn the piano, learn a 2nd language etc)
- Frequent social engagement
- Balanced healthy diet

If you can do that, I personally wouldn't fret over having a drink(s) of your choosing every now and then. I think us APOE4's, especially, get paralysis by analysis that actually leads to a bigger negative impact on us due to stress and anxiety than having a few drinks could ever have.

Main point, don't cut off your nose to spite your face. If having a couple drinks from time to time gives you enjoyment out of life, I wouldn't be overly concerned about the down stream effects if the majority of your day to day habits are all congruent with a healthy lifestyle.

If alcohol is having obvious negative effects on your cognition/life or you find yourself drinking far to frequently, at that point you need to ask yourself if it's worth it but if that isn't happening then I wouldn't be eating myself up over it.

Just my 2 cents on the matter !

[NewRon]

Interestingly, my fasting blood glucose is consistently about 10 points lower, (80 vs 90) the mornings after I've had wine...

[mike]

Instead of putting out glucose over night, your liver is working to clear out the poison . I'm diabetic, and it can work that way as long as there is little sugar, so red wine, not white. Straight liquor, not cocktails with added sugar.

[NewRon]

Mike,

Yes, it's usually red wine (natural wine), preceded by 1200mg of N-Acetyl Cysteine an hour beforehand on an empty stomach, and sometimes during my sipping. It seems it can help protect the liver from some of your earlier mentioned nasties!

[frankiesfriend]

I could not find the research article I referenced in an earlier post on this thread, but I did a little digging and uncovered the following articles, many of which are reviews of research articles on this topic, and have provided quotes from the articles:

H.M. Schipper, “Apolipoprotein E: Implications for AD neurobiology, epidemiology and risk assessment”
in Neurobiology of Aging, 32: 2011: 778 – 790.
"In a subgroup of the NHLBI Twin Study - Carmelli et al. (1999) provided evidence that individuals consuming up to one alcoholic beverage per day on average experienced less cognitive dysfunction, defined as MMSE less than 26 and/or DSS less than 32 and/or BVRT correct less than 5, relative to abstainers (OR: 06, 95% CI: 0.4-0.9). Of note, they observed that the protective effect of light drinking was significant in the presence of genetic risk, i.e. in the APOE-4 positive stratum (RR: 0.5, 0.2 – 0.9), but not in APOE-4-negative subjections (RR: 0.7, 0.4 – 1.3). The authors of this study suggested that light-moderate alcohol ingestion may preferentially protect against cognitive decline in APOE-4 carriers by (a) improving deleterious lipid profiles associated with this genotype and/or (b) curtailing senile plaque formation via direct antagonism of the interaction of the APOE-4 protein with beta-amyloid (Strittmatter et al., 1993)."

Luchinger, J, et. Al. “American Geriatric Society”, 2004, 52:540. “Alcohol Intake and Risk of Dementia”
“Stratified analyses by APOE-e4 allele revealed that, in 667 individuals without the allele, light to moderate intake of wine was associated with a lower risk of dementia (HR50.44, 95% CI50.25–0.77; P5.004), and AD (HR50.45, 95% CI50.24–0.85; P5.013) compared with nondrinkers, whereas this association disappeared for individuals heterozygous or homozygous for the APOEe4 allele (HR for dementia51.10, 95% CI50.59–2.04; P5.093; HR for AD51.32, 95% CI50.67–2.60; P5.427). The interaction terms for alcohol category and the APOE-e4 allele in the models with dementia and AD as outcomes were both statistically significant (P5.056 and P5.032, respectively). No effect modification by sex, diabetes mellitus, hypertension, heart disease, or smoking was found.”
“Analyses stratified by the presence of APOE-e4 also showed that the association between light wine intake and lower risk of AD was restricted to individuals without the APOE-e4 allele whereas in individuals who were heterozygous or homozygous for the allele, there was no association between wine intake and lower risk of AD."

Peters, R., et al. “Age and Ageing”, “Alcohol, dementia and cognitive decline in the elderly: a systematic review. 2008, 37: 505-512.
“At least one study has found that light to moderate alcohol intake (onedrink per week to four drinks per day) is associated with a lower prevalence of vascular brain findings on imaging and less atrophy of the hippocampus and amygdala in APOEe4 carriers as assessed by magnetic resonance imaging”
(This paper Includes reviews of 3 studies with APOE status, generally showing that more than very light drinking is harmful.)

Weyerer, S. et. Al. “Current alcohol consumption and its relationship to incident dementia: results from a 3 year follow up study among care givers 75 years and older. 2011 “Age and Ageing” 40:456-463.
“Alcohol consumption was significantly associated with male gender, younger age, higher level of education, not living alone and not being depressed. No association was found between alcohol consumption and functional impairment, somatic co-morbidity, smoking, MCI or apoE4 status.”

Rehm, et al. “Alcohol Use and Dementia: a systematic scoping review”, 2019. Alzheimer’s Research and Therapy https://alzres.biomedcentral.com/articl ... 018-0453-0
Recently published review includes many studies indicating a reduced risk of dementia with light to moderate alcohol use. Purnell et al, reference #42 provides the following: “Four out of five studies found no association between alcohol use and the incidence of AD. One study reported an association with a decreased risk of AD, in part in interaction with apolipoprotein E ε4.”

World Alzheimer’s Report 2014: Dementia and Risk Reduction – an analysis of protective and modifiable factors.
“There is no evidence that the association between alcohol consumption and dementia is modified by
APOE genotype” – page 51

Xu , Wei (2017) European Journal of Epidemiology, January 2017, 32: 31-42
“Also, we explored whether the association between alcohol intake and ACD was influenced by APOE4 status(Table 3). A total of three studies [2, 3, 29] reported the effect size stratified by APOE4 status, among which the case number in study by Kivipelto et al. [29] was too small and thus excluded. We found a roughly 40% reduction of dementia risk for light drinking or light-to-moderate drinking for APOE4 carriers. Otherwise, the non-significant association for APOE4 non-carriers should be interpreted with caution due to a massive heterogeneity."

Lee, Y. “Systematic Review of Health Behavioral Risks and Cognitive Health in Older Adults” – International Psychogeriatrics (2010) 22:2, 174 – 187.
“There were some inconsistencies in the studies, especially with regard to APOE carrier status,
gender, and alcohol consumption. Differences in the characteristics of the cohorts, such as
racial or ethnic composition and gender (Taaffe et al., 2008), may account for the divergent
findings by APOE status. Moreover, differential mortality, with elevated cardiovascular morbidity
and mortality among APOE carriers, may favor significant associations in non-carriers (Reitz et al.,
2007). The effect of APOE may be so strong that other risk factors do not further contribute to
the relationship. With age, however, the influence of APOE may attenuate (Kivipelto et al., 2008).
Mechanisms by which behavioral risks affect brain function may differ by APOE status. Smoking, in
particular, may have an adverse vascular effect but could be beneficial in APOE carriers by facilitating the release of acetylcholine or increasing the density of nicotinic receptors (Ott et al., 1998; Reitz et al., 2007).
For alcohol consumption, there were conflicting results. Although Ganguli et al. (2005) reported
protective effects of moderate drinking, defined as at least one alcoholic drink per month, on cognitive
function, unfavorable findings were reported in a Finnish study for APOE carriers (Kivipelto et al.,
2008). Binge drinking was a common practice in Finland at the time of midlife assessment. It
has been suggested that APOE carrier status may interact with the binge drinking habit to increase
dementia risk.”

Neafsey, M. et al. “Moderate Alcohol Consumption and cognitive risk” , Review by Edward J. Neafsey, Michael A. Collins, Neuropsychiatric Disease and Treatment, August 2011.
“Analysis also showed that the presence of the apolipoprotein E epsilon 4 allele eliminated the benefit of moderate drinking. However, this was based on a relatively small number of studies and several other studies have found a beneficial effect of the epsilon e4 allele. Further studies are necessary to settle this question.”

(In the discussion section on studies that indicated a negative effect of a given lifestyle or genetic trait on cognitions….)”In summary, 13/23 ratios (57%) in the “worse” group were associated with either heavy drinking (12) or the APOE ε4 allele (1). The remaining ten ratios linking light, moderate, or unknown amounts of alcohol consumption with significantly increased risk of dementia or cognitive impairment represent only 2.2% (10/446) of the total.”

[mike]

I could not find the research article I referenced in an earlier post on this thread, but I did a little digging and uncovered the following articles, many of which are reviews of research articles on this topic, and have provided quotes from the articles:

Except for a couple, I would consider most of these too old to be relevant given the fast pace of AD research. Unless fairly basic research, I would not look at much over 5 years old... When I do Google searches, I tend to try to find stuff within the last year, if possible.

[NewRon]

I would not look at much over 5 years old... When I do Google searches, I tend to try to find stuff within the last year, if possible.

That's also great advice for wine...the younger the wine, the higher the polyphenols

More seriously, Mike, would the damage done by the nasties in the wine be worse than any benefits given by the lower blood sugars? Lowering blood sugars is a major focus here and the wine seems to lower MY blood sugars considerably.
.

[mike]

More seriously, Mike, would the damage done by the nasties in the wine be worse than any benefits given by the lower blood sugars? Lowering blood sugars is a major focus here and the wine seems to lower MY blood sugars considerably.

There is a lot of mixed science out there. My guess is you would be better off spending 30 minutes doing interval training. That being said, I still drink a glass of red wine now and then - I live in Sonoma, after all