Being overweight reduces dementia risk?
The headline on Friday 10th April 2015 was “Being overweight ‘reduces dementia risk’”. The original article is here. Sadly on pay per view only, so it cost me $31.50 for 6 pages.
I tweeted early on Friday morning “Being overweight may be associated with reduced incidence of dementia but ‘reduces risk of’? Really?”
I couldn’t see a plausible mechanism and nor could the researchers, who confessed to having been “surprised”. As the BBC article noted, “Any explanation for the protective effect is distinctly lacking.”
However, twitter being the marvel that it is, served up a plausible mechanism, from a Seattle physician, within minutes of my tweet. We’ll get the study and the usual pitfalls out of the way first and then see what could really be interesting about this finding.
The study was the usual “let’s examine lots of data” format, which is the most common method for grabbing headlines at the moment. Data from almost two million people (1,958,191) was reviewed. The average age at the start of study was 55. The average length of follow-up was 9 years. Hence this was a huge review with almost 20 million person years of data.
There were 45,507 cases of dementia recorded during the follow-up period. The paper presented this as 2.4 cases per 1000 person years (i.e. their calculation, not mine).
BMI (body mass index) was recorded at the start of the study for each participant. This measurement was taken some time between 1992 and 2007 – when the participants reached the age of 40 or older. We know nothing about what happened to weight over the average nine years of follow-up. Those who were underweight at the start of the study could have been obese by the time they developed dementia and vice versa – we know none of this.
The study confirmed that dementia was strongly associated with age and so age needed to be adjusted for in the analysis of the data.
The numbers in the newspaper headlines came from Table 2 in the paper and from the top set of numbers (adjusted for age and sex only). However, even when the researchers adjusted for everything they could think of (smoking, diabetes, medications, alcohol etc) the numbers hardly changed, so we can see these as valid figures.
The Table 2 numbers took normal BMI as “healthy weight” and gave that a reference base of 1.0. They then presented the incident rate of dementia, relative to 1.0, as follows for the different weight categories:
– Underweight (BMI <20) = 1.34 (this was where the “34% higher risk” headlines came from).
– Overweight (25-29.9) = 0.82 (this was where the “18% lower risk” came from).
– Obese (30-34.9) = 0.76 (this was where the “24% lower risk” came from).
– Very obese (BMI >40) = 0.71 (this was where the “29% lower risk” came from).
The common pitfalls
We should know these really well by now:
1) This is association not causation.
We may have observed that people who wore red socks to the baseline health check went on to develop dementia. We should not jump to the conclusion that wearing red socks increases the risk of dementia.
2) This is relative risk, not absolute.
The fact that there were 2.4 cases of dementia per 1,000 person years means that I’m not worried about any of this already. Applying this 2.4 number to the incident rate in each of the different weight groups, results in the following:
– The incident rate for underweight people becomes 3.2 cases per 1,000 person years.
– The incident rate for overweight people becomes 2.0 cases per 1,000 person years
– The incident rate for obese people becomes 1.8 cases per 1,000 person years
– The incident rate for very obese people becomes 1.7 cases per 1,000 person years
2.0 per 1,000 person years vs. 2.4 per 1,000 person years suddenly doesn’t seem quite so dramatic, don’t you think? But those are the actual real, absolute, incident rates behind the headlines.
Possible things going on
It could be the case that more obese people died and were therefore not available for follow-up (and not alive to develop dementia). An interesting study on weight and mortality here was covered in a much more readable way by the brilliant Dr Malcolm Kendrick here. The study showed that obesity was associated with more deaths, but that being overweight wasn’t. Hence, this cannot serve as an explanation for this dementia weight finding, which showed that the incidence of dementia was lower with every increase in weight category they measured from underweight to very obese.
The researchers themselves offered the possible explanation that heavier people may have taken in more nutrients and that some of these may have had mind protection benefits. I’m not sure that there is any evidence for this (and they didn’t seem that convinced by it). When I heard the lead researcher on Radio 4 on Friday morning, he really did hold the view that he was surprised and couldn’t explain the findings.
The plausible mechanism
A Seattle physician, called Theodore Naiman, who tweets as @tednaiman may have been able to help the research team. In response to my “Really?” tweet, questioning plausible mechanism, he replied:
@zoeharcombe Obesity-resistant persons take more glycation damage hit as their adipocytes don’t protect them by sucking up all extra glucose.”
A quite excellent use of 140 characters! If you need a bit more explanation…
If we view the underweight, not unreasonably, as those most resistant to obesity – these are the people not storing excess glucose in fat cells. They are not laying down fat. It could be that they are underweight because they rarely ingest glucose. However, it is likely that the majority of this group do consume glucose, but their underweight status indicates that they are not storing it. The glucose still has to ‘go/stay’ somewhere and it can therefore be found/spend longer in other parts of the body, where we know sugar causes cell damage.
Conversely, the most obese people are extremely good at storing away excess glucose in fat cells. They may find this attribute undesirable, but it is actually very desirable for the body to ensure that potential glucose (glycation) damage can be minimised with glucose being whizzed away into fat cells very efficiently.
We know throughout evolution that the ability to store fat would have given a human a survival advantage. The fleshy people would out-live the lean people in times of scarcity. It would appear that the ability to store fat most efficiently may have benefit in today’s times of plenty – saving us from sugar damage to brain and body alike.
It doesn’t mean, therefore, that we should try to gain weight to avoid dementia. I did an interview with Radio Tees on Friday morning and the presenter, Mike, wondered if this were license to eat biscuits. No! The direction of causation – if this is the actual mechanism – would be that obese people would have natural dementia protection. The obesity would be the indicator that they have this protection – not the cause of it per se.
Now that’s plausible to me! Tiny absolute risk – but plausible!
28 thoughts on “Being overweight reduces dementia risk?”
I’ve read about how hardcore vegans are suffering from depression, suicidal thoughts, anxiety, etc. They are not getting enough fat, animal protein or calories. Not to mention b vitamin deficiencies. Ever notice how violently angry some of them get if you disagree with them, even a little? Shows what is going on (or not going on) in their brains.
To me, the thing that really bringing humanity to its knees is the fact that our conscious mind and subconscious mind are no longer in synch with each other. Our subconscious mind could be screaming at us to eat better, yet because our conscious mind either can refuse to take note and listen, or just not understand it at all, we surrender to denial and shame and “wonder” why we are feeling all of these false moods (irregular moods from lack of nutrition, interference with brain chemistry other necessities that are lacking) when deep down, we KNOW what we need.
All in all, there’s a huge translation error between our two minds. One knows it all, the other just thinks or wants to believe it knows it all.
Zoe: the explanation you write about in the article is logical, and does seem to make sense. I guess something similar might be happening in the case of diabetes; there is a theory that the laying down of fat might be the body’s defense mechanism, by “getting rid of the excess sugar”, in order to stave off diabetes. This may be why overweight is associated with diabetes, but doesn’t necessarily cause it- (in fact, it might prevent it, in the short term). An interesting theory, in any case.
As the study- like all studies- gave results in percentages, as opposed to individual results, I have a few more comments to add:
1) Did they record how many of the overweight/obese people were dieting? It seems logical that a greater percentage of overweight people might try to reduce their weight- (as opposed to the lean people in the study). The low carb diet is a pretty well known and popular diet for weight loss. Since they didn’t follow up to see how many people actually lost weight, it would seem possible that a greater percentage of the overweight people might have been either eating low carb (at least part of the time; there was a 9 year follow up, after all)- or even just reducing sugar intake. Lean people may tend to think they’re getting away with eating sugar and refined carbohydrates, since the damage may not be apparent at first glance, but there may be hidden metabolic problems. If more overweight people were trying to take steps to reduce their weight, this could have in turn made them metabolically healthier (by eating less sugar). Just a possibility…..
2) I’ve read that the vegan diet might also be associated with dementia. It could be possible that a greater proportion of the lean people in the study were not eating animal foods- (though not necessarily; it is possible to be an overweight vegan I guess). On a similar note, low cholesterol is also associated with dementia and other brain problems. Is it likely that the overweight group had higher cholesterol?
Answers to questions :-)
1) There is no record of how many people were dieting at the start of the study or during it – there was a baseline BMI taken and then nothing more. Hence your low carb thought was sadly not tested.
2) An interesting two parter! a) yes – there are overweight vegans – we are seeing an increasing number ask about The Harcombe Diet, which is fine for veggies, but not vegans. Younger and newer vegans can often be underweight in the early days, as so much is cut out of the diet. However, the fact that everything a vegan eats has a carb content, does catch up in time. All the people in this study were over 40 (avg age 55) so I think the underweight/vegan theory is unlikely.
The higher cholesterol theory is very plausible!
Best wishes – Zoe
Too bad they didn’t take what they were eating into consideration, since I’m sure that would be the biggest influence- (more so than BMI, I reckon).
And that’s very interesting, about vegans!
Thanks for your comments,
Dr. Naiman is spot-on, in my opinion. In the research I’ve done into Alzheimer’s as type 3 diabetes, the pathology is largely the result of hyperinsulinemia, glycation damage, and mitochondrial oxidative stress. If people who become overweight suffer less glycation and inflammation because the glucose is cleared out of the bloodstream more rapidly, then it does stand to reason that they would have a lower risk for dementia and cognitive decline.
I’ve linked in another post above, so forgive me for doing so again here, but I am really trying to spread the word about my book, because I am *small potatoes,* and have a very small following. I am trying to get this potentially lifesaving information onto the radar of people with greater influence than I have.
I encourage anyone concerned with this topic to take a look at my book: http://alzheimersantidote.com/
You can download the free sample, which includes the table of contents, so you can see the breadth of topics covered and decide if this will be a helpful resource for you: http://alzheimersantidote.com/docs/Alzheimers-Antidote-Sample.pdf
You will learn *exactly why* hyperinsulinemia/insulin resistance and problems with glucose metabolism in the brain are the foundation of Alzheimer’s pathology, as well as the role of elevated insulin in leading to accumulation of the beta-amyloid plaques. The medical literature is unambiguous on these points. I cover the ApoE4 genotype, the role of cholesterol in the brain, neuron structure & function…no stone left unturned.
Please, anyone who’s interested in this, take a look. I’m happy to answer any questions you might have. This is absolutely critical information, and it’s *not* trickling down to the offices of the average neurologists and family doctors. If it was, I wouldn’t have *had to* write the book.
Zoe, I don’t think Catherine or anyone else should worry about a low BMI, particularly those eating anything like the Harcombe diet.
Three months ago I abandoned the low fat diet that I’d followed for over twenty years. I increased my fat intake and reduced my carbohydrate intake by 80% – 90%. I quickly felt much more energetic and, more interestingly, substantially more mentally alert and positive. It’s like I’ve been issued with new batteries! I’ve been trained to be methodical and evidence based and I would have been hugely sceptical a few months ago if someone had said I’d experience these mental benefits from a change in diet.
I was intrigued and began to search for evidence between a low fat diet and reduced mental health. It didn’t take much effort to find medical literature linking a low fat diet to anxiety and worse. If we are designed to eat fat, which is more than plausible, then it makes sense that limiting a food our brain needs is likely to have adverse effects. I believe Stephanie Seneff from MIT believes the combination of statins and the low fat diet are the most likely cause of Alzeimer’s. Unfortunately, research into the disease always seems to be focused on a drug solution because that’s what the drug industry wants and persuades charities to pursue.
If I generalise and assume that obese people are more likely to have ignored the low fat dogma, might that not explain a reduced incidence of Alzeimer’s? They might have eaten lots of the ‘wrong’ things, but perhaps the fat part of their diet was protective?
There are a number of intriguing reports on the positive benefits of coconut oil on Aklzimer’s and readers might be interested in the following American news item on YouTube.
“However, it is likely that the majority of this group do consume glucose, but their underweight status indicates that they are not storing it. The glucose still has to ‘go/stay’ somewhere and it can therefore be found/spend longer in other parts of the body, where we know sugar causes cell damage.” – Now I am seriously concerned. My BMI is just under twenty (thanks to pretty much living on Phase II of the Harcombe diet very contentedly) but I had no idea I might be damaging myself by storing sugars in the “wrong” cells, there not being so many fat cells available. Is a BMI of say 19.6 a Bad Thing?
Generally a BMI of c. 20 is not a bad thing or a good thing. If at natural weight (as you should be doing what you’re doing ;-)) you are where you are. It would be a bad thing if you developed malaria (like Cheryl Cole) and lost pounds that you didn’t have to lose. In terms of illness, carrying extra is generally a good thing. Sadly – this ‘life insurance policy’ is not valued for looks/appearance.
If you’re doing The Harcombe Diet, you won’t be having anything like the glucose that the average person consumes. And – most importantly – presumably you did it because you had weight to lose. So you showed that you are an efficient storer of fat/glucose when you need to be? You’re now likely one of the minority in the passage you quoted – those not consuming much glucose and thus using, rather than storing, what you do consume.
Keep eating well and don’t worry!
Best wishes – Zoe
Thank you so much Zoe – that was the reassurance I needed. Phase II is so tasty I always forget it probably involves ingesting less glucose than “normal”.
As someone whose mother has Alzheimer’s Disease, I just want to add that any research into how this evil disease, and other forms of dementia, is caused is very welcome. I have read that a number of doctors/scientists consider Alzheimer’s to be “Type III diabetes” and I would love to see more investigation into that. I totally agree, though, Zoe, that this latest headline-grabber is the usual misleading nonsense – it really doesn’t help the cause at all. My mother is now 77, and has been what the BMI bods would term “obese” for most of her adult life, but was always a very healthy woman, rarely getting more than a cold. She did smoke until she was 58. She does seem to have developed much more of a “sweet tooth” in the last 15 years or so, and if she knows there is pudding to follow her main course, will push away the main half eaten, saying she can’t manage any more, then proceeds to devour whatever the pudding is!! Chocolate is her god! Since her diagnosis four years ago, I have tried to read as much as I can about Alzheimer’s, from all sorts of sources as it is my biggest fear, and my sister’s, that one day we might become victims of it, too. It really is the most heart-breaking thing to watch. Here’s to proper, thorough, research, not totally misleading headlines.
Hi Catherine – beautifully put – I’m so sorry to hear about you’re mother and you’re quite right that headline grabbing doesn’t help. If this glucose inference could be connected to the type 3 diabetes (with which I’m also familiar) we may make progress. Only yesterday there were numbers released about barely a few pence out of £10 heading towards dementia research? I didn’t catch the full story or what the pence to £10 reference was but it seemed to be poorly funded.
Best wishes – Zoe
p.s. chocolate is my God too! ;-)
I’m so sorry to hear about your mother’s situation. I’m a low-carb & keto-friendly nutritionist, and I’ve done a great deal of research into the topic of Alzheimer’s as “type 3 diabetes.” In fact, I’ve just (really, *just* — two days ago!) released an e-book with everything you could want to know: where Alz is coming from, why it’s happening, and most important, *what to do about it.* The intervention is multi-faceted, but as you might guess, the primary and foremost step is dramatic carbohydrate reduction. You can check out the book here: http://alzheimersantidote.com/
You can download a free sample to see if it’s something that might be helpful to you and your family. If you’d like to read something that covers most of the basics, hop on over to the Weston A. Price Foundation’s site, where I published an article about this last summer:
I’ve also addressed this on my blog: http://www.tuitnutrition.com/2015/04/alzheimers-antidote.html
I don’t mean to get my book in anyone’s face here, of overly promote it, but I am genuinely trying to get this lifesaving information out to people, because conventional medicine is such an utterly dismal *failure* for Alzheimer’s sufferers and their caregivers, and I am absolutely convinced there is a relatively simple way out of the darkness.
Hi Amy – many thanks for your help for Catherine (and others who may read this). Normally the spam filter knocks out most things with 1 link, let alone 3 – it must have known you were trying to help :-)
Best wishes – Zoe
In that case, I’m glad it got through! :)
Amy, will you be putting your book on Kindle?
Amy – thank you so much for this. Alzheimer’s is something that, to me, everyone is terrified of getting, but far more funding (in my opinion) and publicity (again in my opinion) goes into cancer research. I have no problem with the amount of money and research that goes into cancer, I simply think that Alzheimer’s deserves the same attention. I will be reading all the books/blogs/articles you mention avidly – I think it was something that the wonderful Tom Naughton wrote or quoted that mentioned “Type III diabetes” and this really fired off my interest, as it seemed to make a great deal of sense. You go and get your book in as many faces as you possibly can, you’ll get no complaint from me! Thank you again.
Hi Catherine – just rescued another Amy post from spam – so hope this helps!
Best wishes – Zoe
Really interesting and thought provoking, Zoe and Amy. What astounds me is that this Type III diabetes stuff has been around for over 15 years, so why on earth isn’t the message being given out by all the “experts” and health professionals who deal with Alzheimer’s patients, why aren’t we all being told about this almost as a matter of course? My mother takes a drug called Aricept, which I understand can halt/slow down the progress of the disease, but that there are no guarantees attached. She has been assessed as not having deteriorated for the past two years, so perhaps she is one of the luckier ones in this respect. However, when you think that a change of diet might have the same, if not even better, effect, I think I would prefer to opt for the change of diet, rather than medication. Hang on a sec – the Type III diabetes thing might mean that drugs aren’t needed in future – there’s my answer as to why we’re not all generally told about it……!!!! Or am I just a cynic?
First port of call when looking for paywalled papers is hit up LibGen, eg I just put the DOI number into there and got the PDF for free:
There’s other options via Twitter and Reddit where you’ll often get someone with access to sort you out.
Hope that helps…
Many thanks for this! As an author, I do try to respect copyright – I just wish the journals would charge less. $31 for 6 pages or entire books for less than a third of that! Just seems a bit steep.
Thirty-one dollars for 6 pages is ridiculous, particularly for association studies. Apparently, according to Tom Naughton, four out of five ‘association’ studies later turn out to be wrong. Worth bearing in mind when these studies hit the headlines, and confuse and disillusion the public.
it is also worth noting that BMI calculations are not exactly rooted in science – perhaps being “overweight” is actually more healthy than we are led to believe.
Absolutely! This article from the weekend (annoyingly behind the firewall) http://www.thesundaytimes.co.uk/sto/newsreview/features/article1542377.ece had a cartoon about BMI at the top “Being Mostly Invented”!
I wonder if there’s an additional filter in place: if the overweight/obese who *don’t* efficiently store glucose in fat (i.e. have similar glycation issues to the underweight in Naiman’s hypothesis), would the combination of obesity and glycation factors perhaps cause them to die of other problems before dementia sets in? That could potentially artificially lower the incidence of dementia in overweight/obese by removing the highest-risk individuals before they have a chance to exhibit symptoms.
This is way beyond my understanding, though.
The usual glycation measure is the “long blood sugar”, glycated hemoglobine A1c. In the literature it indicates the average blood sugar levels for 6–8 weeks.
Do you know if there are tests that measure the glycation damage from longer period?
Hi there – I’m no expert in this area. Glynthincs (tweets as @Cholesterol_OK) is someone I turn to on glycation.
I do recall the work of Prof Cynthia Kenyon being really interesting in this area. (http://www.science-of-aging.com/timelines/kenyon-elegans-mutant-lives-twice-as-long.php) She seems to have identified genes mutating with glycation damage.
Best wishes – Zoe
Kenyon’s work is one of the things that prompted me to go from half-ass low carb to ketogenic (and nowadays pretty much zero carb/super high fat), me and a mate did a fun podcast on her stuff in 2011:
Hi Ash – many thanks for this – I didn’t realise CK was heading down the drug route – makes sense – but it would be so nice for someone not to sell out. Aim for the Nobel prize – not the lottery!
Bye for now – Zoe