Bread & Weight Gain/Loss: What’s The Truth?
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It’s Q&A Day at 10almonds!
Have a question or a request? We love to hear from you!
In cases where we’ve already covered something, we might link to what we wrote before, but will always be happy to revisit any of our topics again in the future too—there’s always more to say!
No question/request too big or small 😎
❝Every now and again I try quitting bread to lose some weight and it works, but it always seems to come back and then I eat bread again anyway. Is there a way to break out of this cycle?❞
Yes! You can break out of that cycle by simply enjoying bread in moderation without quitting (and then you will certainly not be in the cycle of quitting it and restarting it).
However, to give an answer that’s probably more in the spirit of your question:
Firstly, know that a lot of the short-term benefits of quitting bread are unrelated to fat loss. We’ve covered this part before, and in few words:
Cutting bread for 30 days can lead to weight loss for some people, but the initial change is often more a matter of reduced water retention and bloating rather than immediate fat loss. In particular, it’s common for people feel lighter within the first week or so because reducing fermentable carbohydrates can decrease gas production and resultant digestive discomfort, especially in those with sensitive guts.
You can read more about this, here: Does Quitting Bread For 30 Days Trigger Weight Loss?
Next, understand that oftentimes the issue is not the bread, so much as the glycemic index thereof, and this can vary wildly from one bread to another.
We wrote about this, here: Is Flour As Bad As Sugar?
And more broadly, here: Grains: Bread Of Life, Or Cereal Killer?
Lastly (for today), there’s some recent science that indicates the issue with bread is actually in your non-bread dietary components.
Researchers (Dr. Miona Marutani et al.) found that mice given access to carbohydrate-heavy foods like bread, rice, and wheat strongly preferred them over standard mouse food and gained body fat despite eating roughly the same number of calories.
In other words, the body fat gain wasn’t about eating more bread; it was about eating less of the other food!
You can read the paper itself, here: Wheat Flour Intake Promotes Weight Gain and Metabolic Changes in Mice
Now, this was a mouse study and may or may not be replicated in humans, but it at the very least presents us with an important reminder of the value of positive dieting, that is to say, worrying less about what to exclude from our diets, and more about what to include, to ensure we get good, diverse, nutrient coverage.
Yes, even if your goal is fat loss, making conscious choices about what to include, rather than what to exclude, can help a lot.
For more on that, enjoy: Intuitive Eating Might Not Be What You Think
Want to enjoy bread, healthily?
As we’ve said, moderation is key, as we as a focus on making sure to include plenty of good nutrients.
There are several ways to do this, including:
- A healthy sandwich with lots of nutritious things inside!
- Healthy things on toast (avocado toast is a great example)
- Soup with bread (just make sure there’s plenty of healthy stuff in the soup!)
Another approach (which can be done in tandem with the above) is to make healthier, non-wheat bread, for example:
- “4-Ingredient 10-Minute Bread” That’s High-Protein, High-Fiber, Gluten-Free
- Healthy Homemade Flatbreads ← a different healthy bread recipe of ours
- Delicious Quinoa Avocado Bread ← another one, also in text
Enjoy!
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Alzheimer’s may have once spread from person to person, but the risk of that happening today is incredibly low
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An article published this week in the prestigious journal Nature Medicine documents what is believed to be the first evidence that Alzheimer’s disease can be transmitted from person to person.
The finding arose from long-term follow up of patients who received human growth hormone (hGH) that was taken from brain tissue of deceased donors.
Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards – including in Australia from the mid 60s.
The practice stopped in 1985 when it was discovered around 200 patients worldwide who had received these donations went on to develop Creuztfeldt-Jakob disease (CJD), which causes a rapidly progressive dementia. This is an otherwise extremely rare condition, affecting roughly one person in a million.
What’s CJD got to do with Alzehimer’s?
CJD is caused by prions: infective particles that are neither bacterial or viral, but consist of abnormally folded proteins that can be transmitted from cell to cell.
Other prion diseases include kuru, a dementia seen in New Guinea tribespeople caused by eating human tissue, scrapie (a disease of sheep) and variant CJD or bovine spongiform encephalopathy, otherwise known as mad cow disease. This raised public health concerns over the eating of beef products in the United Kingdom in the 1980s.
Human growth hormone used to come from donated organs
Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue.
But because the amount of hGH contained in a single gland is extremely small, any single dose given to any one patient could contain material from around 16,000 donated glands.
An average course of hGH treatment lasts around four years, so the chances of receiving contaminated material – even for a very rare condition such as CJD – became quite high for such people.
hGH is now manufactured synthetically in a laboratory, rather than from human tissue. So this particular mode of CJD transmission is no longer a risk.
Human growth hormone is now produced in a lab.
National Cancer Institute/UnsplashWhat are the latest findings about Alzheimer’s disease?
The Nature Medicine paper provides the first evidence that transmission of Alzheimer’s disease can occur via human-to-human transmission.
The authors examined the outcomes of people who received donated hGH until 1985. They found five such recipients had developed early-onset Alzheimer’s disease.
They considered other explanations for the findings but concluded donated hGH was the likely cause.
Given Alzheimer’s disease is a much more common illness than CJD, the authors presume those who received donated hGH before 1985 may be at higher risk of developing Alzheimer’s disease.
Alzheimer’s disease is caused by presence of two abnormally folded proteins: amyloid and tau. There is increasing evidence these proteins spread in the brain in a similar way to prion diseases. So the mode of transmission the authors propose is certainly plausible.
However, given the amyloid protein deposits in the brain at least 20 years before clinical Alzheimer’s disease develops, there is likely to be a considerable time lag before cases that might arise from the receipt of donated hGH become evident.
When was this process used in Australia?
In Australia, donated pituitary material was used from 1967 to 1985 to treat people with short stature and infertility.
More than 2,000 people received such treatment. Four developed CJD, the last case identified in 1991. All four cases were likely linked to a single contaminated batch.
The risks of any other cases of CJD developing now in pituitary material recipients, so long after the occurrence of the last identified case in Australia, are considered to be incredibly small.
Early-onset Alzheimer’s disease (defined as occurring before the age of 65) is uncommon, accounting for around 5% of all cases. Below the age of 50 it’s rare and likely to have a genetic contribution.
Early onset Alzheimer’s means it occurs before age 65.
perfectlab/ShutterstockThe risk is very low – and you can’t ‘catch’ it like a virus
The Nature Medicine paper identified five cases which were diagnosed in people aged 38 to 55. This is more than could be expected by chance, but still very low in comparison to the total number of patients treated worldwide.
Although the long “incubation period” of Alzheimer’s disease may mean more similar cases may be identified in the future, the absolute risk remains very low. The main scientific interest of the article lies in the fact it’s first to demonstrate that Alzheimer’s disease can be transmitted from person to person in a similar way to prion diseases, rather than in any public health risk.
The authors were keen to emphasise, as I will, that Alzheimer’s cannot be contracted via contact with or providing care to people with Alzheimer’s disease.
Steve Macfarlane, Head of Clinical Services, Dementia Support Australia, & Associate Professor of Psychiatry, Monash University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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The Simple Six – by Clinton Dobbins
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We at 10almonds don’t believe in keeping things a mystery, so…
“The Simple Six” are:
- the squat
- the goblet squat
- the hinge
- the kettlebell swing
- the push
- the push-up
- the kettle-bell press
- the pull
- the chin-up
- the gait, and
- walking.
Ok, we’re being a little glib here because to be fair, those are chunked into six groups, but the point is: don’t let the title fool you into thinking the book could have been an article; there’s plenty of valuable content here.
That said, it is a short book (64 pages), but with an average of 10 pages per exercise type, it’s a lot more than for example we could ever put into our newsletter.
Bottom line: we know that 10almonds readers like simple, clear, evidence-based, to-the-point health information, and that’s what this book is, so we do recommend it.
Click here to check out The Simple Six, and streamline your workouts!
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Green Coffee Bean Extract: Coffee Benefits Without The Coffee?
10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.
Coffee is, on balance, very good for the health in moderation. We wrote about it here:
The Bitter Truth About Coffee (or is it?)
Some quick facts before moving on:
- Coffee is the world’s biggest source of antioxidants
- 65% reduced risk of Alzheimer’s for coffee-drinkers
- 67% reduced risk of type 2 diabetes for coffee-drinkers
- 43% reduced risk of liver cancer for coffee-drinkers
- 53% reduced suicide risk for coffee-drinkers
Those are some compelling statistics!
But what about the caffeine content?
Assuming one doesn’t have a caffeine sensitivity, caffeine is also healthy in moderation—but it is easy to accidentally become dependent on it, so it can be good to take a “tolerance break” once in a while, and then reintroduce it with more modest moderation:
Caffeine: Cognitive Enhancer Or Brain-Wrecker?
We also, for that matter, have discussed its impact on the gut:
Coffee & Your Gut ← surprise, it’s a positive impact
What if I don’t like coffee?
We suspect that, having seen the title of this article, you know what the answer’s going to be here:
Green coffee bean extract is the extract from green (i.e. unroasted) coffee beans. It has one or two advantages over drinking coffee:
- For those who do not like drinking coffee, this supplement sidesteps that neatly
- Roasting coffee beans destroys a lot (sometimes almost all; it depends on the temperature and duration) of their chlorogenic acid, a highly beneficial polyphenol; using unroasted (i.e. green) coffee beans avoids that
See: Role of roasting conditions in the level of chlorogenic acid content in coffee beans
All about GCE and CGA
That’s “green coffee extract” and “chlorogenic acid”, respectively, bearing in mind that the latter is found generously in the former.
As to what it does:
❝CGA is an important and biologically active dietary polyphenol, playing several important and therapeutic roles such as antioxidant activity, antibacterial, hepatoprotective, cardioprotective, anti-inflammatory, antipyretic, neuroprotective, anti-obesity, antiviral, anti-microbial, anti-hypertension, free radicals scavenger and a central nervous system (CNS) stimulator. Furthermore, CGA causes hepatoprotective effects.❞
👆 Those are the things we know for sure that it does. And it may do even more things:
❝In addition, it has been found that CGA could modulate lipid metabolism and glucose in both genetically and healthy metabolic related disorders. It is speculated that CGA can perform crucial roles in lipid and glucose metabolism regulation and thus help to treat many disorders such as hepatic steatosis, cardiovascular disease, diabetes, and obesity as well.❞
Read in full: Chlorogenic acid (CGA): A pharmacological review and call for further research
About lipid metabolism…
- Green coffee extract supplementation significantly reduces serum total cholesterol levels.
- Green coffee extract supplementation significantly reduces serum LDL (“bad” cholesterol) levels.
- Increases in HDL (“good” cholesterol) after green coffee bean extract consumption are significant in green coffee bean extract dosages ≥400mg/day.
About blood glucose and insulin…
- Green coffee extract supplementation significantly improved fasting blood sugar levels
- Green coffee extract supplementation at ≥400 mg/day significantly lowered postprandial insulin levels (that’s good)
Want to try some?
We don’t sell it, but here for your convenience is an example product on Amazon 😎
Enjoy!
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Visceral Fat: Why It Matters & How To Improve It
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Dr. Ruth Machin demystifies it:
At the core of things
Visceral fat is fat stored deep inside your abdominal cavity, underneath your abdominal wall muscles, surrounding your organs. As such, it’s different from subcutaneous fat (under your skin, the fat you can squish from the outside), and belongs to the broader category of ectopic fat (ectopic = “out of place”).
While it’s fine for your organs to have a little padding, the problem with excess visceral fat is that it secretes pro-inflammatory adipokines that drive insulin resistance, raise the risk of type 2 diabetes, promote hypertension, contribute to heart disease, and generally bring about (or exacerbate) metabolic syndrome in general.
Although overall weight gain in midlife comes mostly from age and reduced activity, not menopause itself, menopause is a factor—because declining estrogen levels result in the body shifting fat storage from hips and thighs, towards your midsection, increasing visceral fat.
How to measure visceral fat: it cannot be seen externally; waist-to-height ratio is a better guide than BMI; thresholds above 0.5 signal increased risk; imaging such as MRI is required for accurate measurement in research.
Still, if you have a smart scale, it’ll do a decent estimate for you as part of its body composition test, based on conductivity. Just remember, it’s not accurate, so in that case, worry less about the actual numbers, and more about the trends (e.g. whether the visceral fat score is going up or down over time or remaining the same).
Some notes from Dr. Machin on dietary considerations:
- Diet quality for reducing visceral fat: research shows that a mild (!) calorie deficit combined with avoiding saturated fats but enjoying low-GI carbohydrates (i.e: get plenty of fiber with your carbs) reduces visceral fat.
- Whole-food approaches that work: both low-carb and higher carb diets with unprocessed foods reduce visceral fat; avoiding added sugars and refined carbohydrates improves insulin resistance and abdominal fat patterns. No surprises here.
- Why the Mediterranean diet is effective: it promotes whole grains, beans, legumes, olive oil, fish, fruit, vegetables, and nuts; it supports cardiovascular health and reduces visceral fat more effectively than low-fat or low-carb diets in the long term.
- Extra benefits from polyphenols: the green Mediterranean diet, enriched with walnuts, green tea, and other polyphenol-dense foods, produced larger visceral fat reductions than the standard Mediterranean diet in clinical trials.
- Foods rich in polyphenols to include: dark berries, green and black tea, nuts with skins (e.g. almonds!), extra virgin olive oil, cocoa, ground flaxseed, red onions, dark green vegetables, and soy; these all improve waist circumference and metabolic markers.
- Overall eating guidance: enjoy unprocessed whole foods, keep added sugars low, avoid sugary drinks especially, replace refined carbohydrates with whole grains, and aim for a diet you can maintain for decades rather than weeks.
For more on all of this, enjoy:
Click Here If The Embedded Video Doesn’t Load Automatically!
Want to learn more?
You might also like:
Visceral Belly Fat & How To Lose It
Take care!
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How Many Heartbeats Do You Have Left?
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Our life is, of course, not literally measured in heartbeats—or at least not usefully so (since there are many other factors). However, there is a strong inverse correlation between resting heartrate and healthy longevity! That is to say, the slower your heart beats, the longer you’ll live.
Caveat: this is a generalization, and applies to a low resting heart rate that is the result of good cardiac health. It does not mean you should, for example, take up the use of heroin for its heartbeat-slowing effects. That will not help you to live longer!
Where’s the science?
Lest our opening claim there sound like popular wisdom rather than something backed by good science, let’s tend to that before moving on to the main thing today. There are, in fact, many papers to back up this claim, but here’s a good one:
It’s a 30-year longitudinal cohort study with 5,070 participants and baseline (as with most longitudinal studies, not everyone survived for the entire duration), and why we particularly like this one is not just its strong statistical significance, but also, because rather than simply looking at average resting heartrate and longevity, it also looked at changes in average resting heartrate and longevity, which makes the case for the link being causal much stronger.
❝In this study, we examined the association between resting heart rate and lifespan using linear regression in the Paris Prospective Study I, the Whitehall I Study, and the Framingham Heart Study. We used Cox proportional hazards regression to relate changes in heart rate over years to mortality risk.
We observed a statistically significant association between increases in resting heart rate over a 5-year period and risk of mortality in the Paris Prospective Study I (HR mortality per 10 bpm increase over time: 1.20; 95% CI: 1.13 to 1.27) and over an 8-year period in the Framingham Heart Study (HR: 1.13; 95% CI: 1.07 to 1.19 for men and HR: 1.09; 95% CI: 1.04 to 1.15 for women), after adjusting for classical risk factors and resting heart rate.
Our study shows that men and women who increase their resting heart rate over time increase their risk of mortality.❞
You may be wondering: why did we say 30 years, if the abstract is citing 5 years and 8 years?
And the answer is: it has to do with the statistical modeling used; the participants were followed for up to 30 years, but the statistical analysis allows us to look at what difference a change in resting heartrate makes over the course of 5 or 8 years, which is more illustrative for most people than “this is what will probably happen when you are [your age plus another 30 years]” statements. Indeed, the very fact that we can see a statistically significant change in mortality risk in just 5 years, makes it clear how big that risk is.
And how big is the risk? Translating the hazard ratios into percentages, we’re looking at, per 10 bpm increase over time, a 20% increase in mortality risk in the 5-year period per the Paris Prospective Study, or a 10%-ish increase in mortality risk in the 8-year period per the Framingham Heart Study. As for why the 5-year period has a bigger risk than the 8-year period, it’s likely down to a slightly different methodology and what other risk factors were controlled for.
One final note: about that “…and resting heart rate”, lest that seem confusing, we will mention that this too was controlled for because the primary input variable being looked at was the change in resting heartrate, not the resting heartrate itself.
In summary: if your resting heartrate increases, so does your mortality risk, at a rate of 10–20% over 5–8 years, for every 10 bpm increase (in other words: that stacks!).
So, what’s this about how many heartbeats we have left?
Based on the above, we can infer that since a change in heartrate is associated with an inverse change in longevity, the total number of heartbeats may often not change much, it’s just that the shorter-lived people squoze more heartbeats into less time.
With that in mind, a “common sense” logic tells us that we should conserve our heartbeats in order to live longer. This is somewhat consistent with the ideas behind some meditative practices.
However, while in a sense that’s not wrong (and such meditative practices can indeed help extend healthy lifespan), this presents an apparent paradox:
Should we avoid exercise, because it accelerates our heartrate while we are exercising?
And the robust answer is no, as some recent science by Dr. Kristel Janssens et al. shows clearly.
How it works: while exercise indeed speeds up the heartrate while exercising, it also lowers one’s resting heartrate by a sufficient amount (per metabolic equivalent of task minutes), that when all’s said and done, the hearts of those who regularly exercise beat fewer times per day than those who do not regularly exercise—and the difference isn’t small:
❝Athletes had an average heart rate of 68 beats per minute (bpm), while non-athletes had 76bpm. That translates to a total of 97,920 beats per day for athletes and 109,440 beats per day for non-athletes – around 10 percent less.❞
Note: that’s average heartrate, not average resting heartrate*. So it’s still counting all the heartbeats that happened during exercise, too. The athletes’ hearts were simply beating slowly enough the rest of the time to more than compensate.
*This is also worth bearing in mind because 68 bpm would be an astonishingly high resting heartrate for a very fit person.
Read the paper in full, here: Balancing Exercise Benefits Against Heartbeat Consumption in Elite Cyclists
Want to do more for your heart?
Check out:
How To Improve Your Heart Rate Variability
…for another thing to bear in mind (and helpfully, it’ll usually lower your resting heartrate, too).
Enjoy!
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Mosquitoes can spread the flesh-eating Buruli ulcer. Here’s how you can protect yourself
10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.
Each year, more and more Victorians become sick with a flesh-eating bacteria known as Buruli ulcer. Last year, 363 people presented with the infection, the highest number since 2004.
But it has been unclear exactly how it spreads, until now. New research shows mosquitoes are infected from biting possums that carry the bacteria. Mozzies spread it to humans through their bite.
What is Buruli ulcer?
Buruli ulcer, also known as Bairnsdale ulcer, is a skin infection caused by the bacterium Mycobacterium ulcerans.
It starts off like a small mosquito bite and over many months, slowly develops into an ulcer, with extensive destruction of the underlying tissue.
While often painless initially, the infection can become very serious. If left untreated, the ulcer can continue to enlarge. This is where it gets its “flesh-eating” name.
Thankfully, it’s treatable. A six to eight week course of specific antibiotics is an effective treatment, sometimes supported with surgery to remove the infected tissue.
Where can you catch it?
The World Health Organization considers Buruli ulcer a neglected tropical skin disease. Cases have been reported across 33 countries, primarily in west and central Africa.
However, since the early 2000s, Buruli ulcer has also been increasingly recorded in coastal Victoria, including suburbs around Melbourne and Geelong.
Scientists have long known Australian native possums were partly responsible for its spread, and suspected mosquitoes also played a role in the increase in cases. New research confirms this.
Our efforts to ‘beat Buruli’
Confirming the role of insects in outbreaks of an infectious disease is achieved by building up corroborating, independent evidence.
In this new research, published in Nature Microbiology, the team (including co-authors Tim Stinear, Stacey Lynch and Peter Mee) conducted extensive surveys across a 350 km² area of Victoria.
We collected mosquitoes and analysed the specimens to determine whether they were carrying the pathogen, and links to infected possums and people. It was like contact tracing for mosquitoes.
Aedes notoscriptus was the mosquito identified as carrying the bacteria that caused Buruli ulcer.
Cameron Webb (NSW Health Pathology)Molecular testing of the mosquito specimens showed that of the two most abundant mosquito species, only Aedes notoscriptus (a widespread species commonly known as the Australian backyard mosquito) was positive for Mycobacterium ulcerans.
We then used genomic tests to show the bacteria found on these mosquitoes matched the bacteria in possum poo and humans with Buruli ulcer.
We further analysed mosquito specimens that contained blood to show Aedes notoscriptus was feeding on both possums and humans.
To then link everything together, geospatial analysis revealed the areas where human Buruli ulcer cases occur overlap with areas where both mosquitoes and possums that harbour Mycobacterium ulcerans are active.
Stop its spread by stopping mozzies breeding
The mosquito in this study primarily responsible for the bacteria’s spread is Aedes notoscriptus, a mosquito that lays its eggs around water in containers in backyard habitats.
Controlling “backyard” mosquitoes is a critical part of reducing the risk of many global mosquito-borne disease, especially dengue and now Buruli ulcer.
You can reduce places where water collects after rainfall, such as potted plant saucers, blocked gutters and drains, unscreened rainwater tanks, and a wide range of plastic buckets and other containers. These should all be either emptied at least weekly or, better yet, thrown away or placed under cover.
Mosquitoes can lay eggs in a wide range of water-filled items in the backyard.
Cameron Webb (NSW Health Pathology)There is a role for insecticides too. While residual insecticides applied to surfaces around the house and garden will reduce mosquito populations, they can also impact other, beneficial, insects. Judicious use of such sprays is recommended. But there are ecological safe insecticides that can be applied to water-filled containers (such as ornamental ponds, fountains, stormwater pits and so on).
Recent research also indicates new mosquito-control approaches that use mosquitoes themselves to spread insecticides may soon be available.
How to protect yourself from bites
The first line of defence will remain personal protection measures against mosquito bites.
Covering up with loose fitted long sleeved shirts, long pants, and covered shoes will provide physical protection from mosquitoes.
Applying topical insect repellent to all exposed areas of skin has been proven to provide safe and effective protection from mosquito bites. Repellents should include diethytolumide (DEET), picaridin or oil of lemon eucalyptus.
While the rise in Buruli ulcer is a significant health concern, so too are many other mosquito-borne diseases. The steps to avoid mosquito bites and exposure to Mycobacteriam ulcerans will also protect against viruses such as Ross River, Barmah Forest, Japanese encephalitis, and Murray Valley encephalitis.
Cameron Webb, Clinical Associate Professor and Principal Hospital Scientist, University of Sydney; Peter Mee, Adjunct Associate Lecturer, School of Applied Systems Biology, La Trobe University; Stacey Lynch, Team Leader- Mammalian infection disease research, CSIRO, and Tim Stinear, Professor of Microbiology, The University of Melbourne
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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