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The effects of fruit - study

HSSS

HSSS

Expert
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7,675
Location
South of England
Type of diabetes
Type 2
Treatment type
Diet only
https://pubmed.ncbi.nlm.nih.gov/35710164/

the effects of at least 4 servings of fruits daily verses less than 2 servings/day on patients with NAFLD. I accept not all of us have this but many type 2 do and the results are interesting regardless I believe. I believe this supports the argument fruit is not good for the liver in anything other than small amounts. (I can’t get to the full article to find which fruits etc were used)

Results include glucose (115.5 ± 30.0 vs. 97.7 ± 19.0, p < .01), and insulin resistance (7.36 ± 4.37 vs. 2.66 ± 1.27, p < .001), and lower HDL (41.4 ± 8.9 vs. 53.8 ± 15.1, p < .001) compared to the control group. Adjusting for BMI and calorie intake did not change the results.

Conclusion:
The results of the present study indicated that consumption of fruits more than 4 servings/day exacerbates steatosis, dyslipidemia, and glycemic control in NAFLD patients. Further studies are needed to identify the underlying mechanisms of the effects of fruits on NAFLD.
 
Good to know, as I've just started to attempt carnivore diet for the second time.
 
Interesting, I'd love to know how big a serving is?
 
EllieM said:
Interesting, I'd love to know how big a serving is?
Click to expand...
Me too but haven’t got to the original study in a free way yet…. I’m assuming at this point 1 apple 1 orange 1 handful of berries as is usual. Though which fruit is also quite relevant.
 
There is inportant information missing from this abstract which makes acceptance of their conclusions difficult. Their results do indeed make claims that other reports did not find, so we need to know why the methodology of this study might affect the outcome. I am minded that the average BMI increased on the FRD which is the opposite of what is normally claimed in other studies. The figures for ALT are suspicious and may be a typo. The TC values went up by more than the LDL raised and HDL lowered, but no check on Trigs is recorded.
How was steatosis measured? other studies use ultrasound scans or modified MRI scans to determine steatosis but their method is not mentioned.

Apart from the extra fruit portions were the diets and timings of the two groups compatible. Over 6 months that is some feat unless the cohort was in an institution where food was controlled.

There seems to be no HbA1c checks so were any of the paricipants diabetic at the start or became diabetic as a result. The rise in fasting glucose might indicate a trend.

I am minded of a trial performed on South Korean monks compared to RC nuns. The monks were vegetarian, the nuns were omnivore. The monks noted a significant rise in obesity and diabetes compared to the nuns, so the study concluded that a vegetarian diet was causing these side effects. Independent analysis of this study established that one significant difference between the groups was that the monks begged for their food during the day. They were fasting during this activiry but were permitted liquid refreshment as they begged. The monks chose to sip on soda pop and this is a probable cofounder that negated the study conclusions.

Since the study is Iranian, one of the fruits may be figs or dates which may be significant in itself. Also a custom in that area is to drink tea heavily sugared, so was this checked?
 
The study in the OP actually slips nicely into my echo chamber, so I am happier now that I have found the full report, which answers most of my queries. We still do not know what fruits were involved or precisely what 7 servings a day actually comprises. They did not check for diabetes, but the change in insulin and fasting glucose seem to be consistent with the change in BMI and waist circumference.

The ALT at 6 months still seems strange. Normal range for ALT is 5 to 60 and cannot go negative. so ALT (89.1 ± 92.9 vs. 32.0 ± 19.2,) seems incorrect or a major problem indeed. But ALT is actually a poor indicator of liver damage since it is like a fingerprick test in that it is a spot check on a moving target.

Trigs were measured and increased on the FRD.

The FBG average only rose to 6.42 mmol/l so not diabetic

They used ultrasound to determine steatosis and liver size and they were careful to select baseline applicants that showed a midrange resolution of NAFLD to ensure best observation of this. It is interesting that most of the FRD group ended up with their liver increasing size to become Large. This is quite telling,

As they point out in the report,all participants started with NAFLD present, and were probably encouraged to follow a NAFLD treatment plan, so weight loss was expected for all of them, but the FRD group gained weight instead even though their sugar intake reduced.
 
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EllieM said:
Interesting, I'd love to know how big a serving is?
Click to expand...
@EllieM The folowin pix is from the Diabetes Australia Circle winter magazine which caters for all makes and models of diabetes.

It's helpful for some amd not others.

Edit: typo

Y9Griul.jpg
 
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Riva_Roxaban said:
@EllieM The folowin pix is from the Diaberes Australia Circle winter magazine which caters for all makes and models of diabetes.

It's helpful for some amd not others...

Y9Griul.jpg
Click to expand...

Yummy! So the fructose is roughly half the carb count. From what I understand, the human body only stores enough enzymes to handle about 40grams, otherwise it’s sent to the liver.

I have some sort of fruit every day, usually just before I head out for my morning walk.
 
LaoDan said:
Yummy! So the fructose is roughly half the carb count. From what I understand, the human body only stores enough enzymes to handle about 40grams, otherwise it’s sent to the liver.

I have some sort of fruit every day, usually just before I head out for my morning walk.
Click to expand...
This article seems to affirm the 40gms level
https://www.houseofwellness.com.au/health/nutrition/fructose-weight-gain-bloating

Healthline in general agrees with the findings, but ends up stating that it is almost impossible to overdose the fructose by eating fruit, and says the jury is still out and nothing conclusive has been found to date.
https://www.healthline.com/nutrition/is-fruit-good-or-bad-for-your-health

I would suggest that the OP study does provide credible evidence for fruit alone being responsible for making existing NAFLD worse. The OP does not demonstrate that eating fruit causes NAFLD.
 
The other thing I would like to add, what was the rest of their diet. @Oldvatr did supply the more detailed study. I noticed the meat consumption went up a little after 3 months in the FRD group, although the fats were even between the two. So I am thinking the fats were not inclusive of the added meat fat or types of meat eaten. I just know high carbs and high fat does not do well together. But very distinctive is the FRD group ate more calories, probably a lot of that from the extra fruit. Of course they were told to........so they added on fruit to meet the diet requirements? And hence ate more? It could also be fruit went down easier and didn't fill up people so they ate more? Especially dried fruit which is like juice and way to easy to eat more than you would the whole fruit. Dried fruits and "other" fruits were a lot higher in FRD group. But after the first month sugars were about the same between the two groups, so they did not include the fruit sugars as part of "sugars". So I am really wondering if the FRD group fit into that high carb high fat category?

It's not just high fruit as I know a few people that do high carb and low fat and they are definitely not insulin resistant. One directly changed from a Bernstein diet, but they all went to needing half the amount of insulin and eating a lot more carbs. I know type 2 can be different, but this study was done on non diabetics so....

There are just a lot of holes it feels like in this study that leaves questions. A little meat consumed, more fruit consumed, but near the same in other groups of food. But more calories means weight gain and weight gain causes more insulin resistance. I think to have a better understanding if fruit is what caused an issue, you would need to keep the calories the same in both groups. It just sounds to me like it's very possible that people added extra calories in extra fruit to meet that 4 plus a day requirement and hence gained weight.
 
I think what the study shows is that fruit in moderation does not make NAFLD worse since the non FRD group ate some fruit, lost weight, and improved the hepatic markers. It is the excess consumption of fruit that made NAFLD markers worse. Yes the increased fruit gave increased calories, but the main mechanism at play is the fact that fructose goes straight to the liver and does not get converted into blood glucose, where it gets converted into trigs for storing in adipose tissue. So fructose is not sugar as nutrition labels define since that is sugars that turn into glucose in the blood. Fructose is simple carbs and only turns into glucose as a result of gluconeogenesis, where trigs are retrieved from storage and converted under the action of glucagon.

It has been suspected for some time that an excess of calories combined with a high fructose load is associated with NAFLD, so a high carb diet with high fructose content is probably one to avoid especially if there is a concerted effort to store excess glucose due to medications to overcome iR. Indeed recent discovery of another enzyme trigger on the alpha cells that operates when there is high blood glucose + high insulin and this condition triggers another pathway in the pancreas to increase insulin output to force storage of fructose to occur. ( it seems to be aimed at fructose since glucose is high and insulin is not storing it away in the normal places. It is believed that this extra boost is what is forcing trig storage into the ectopic adipose tissue in the liver, otherwise known as steatosis) The study does confirm that the livers of the FRD group bloated up into the Large category. This does not appear to be due to the slight increase in meat consumption, which is mainly protein and not stored in the liver.

The danger is not so much fruit intake that is the problem, it is the dried fruit, and the HFCS additive, and also maltodextrin and other sugar alcohols that hide in modern foods. Emulsified starches such as MSG and other flavourings too. These starch derived carbs do not have the fibre content and are highly processed and refined.
 
Fructose going straight to the liver might not be entirely correct, there’s other tissues that have GLUT5 receptors.
from what I understand, it’s the excess that goes to the liver. Dose response?

I could be wrong though.
 
No, you are correct. GLUT5 is in most cells in the body. The small intestine has most for the transport of fructose into the blood. We apparently use fructose a lot while we are in infancy , puberty, and early adulthood, but less as we mature. The main tissues that accept fructose are the kidneys (for fructose recovery and recycling) mammary glands, and testes. It has been dicovered that the brain cells have GLUT5 receptors, but uptake is very low (proven by radiomarked fructose experiments), and appears to be a mechanism for clearing low levels of fructose leaking across the brain barrier. The general purpose of the GLUT5 receptor seems to be to allow gluconeogenesis to occur in muscle and adipose cells and requires insulin as well.

Fructose has not been associated with the Citric cycle so is not used by mitochondria cells for ATP generation directly.

It seems that the contribution of skeletal muscles and of adipocytes in the clearance from the blood and in metabolism of fructose is minor compared with that of the liver and the kidney.

It seems that GLUT5 activity increases in response to cancer and there is ongoing research in this aspect. It is not alone, as most glucose transporters also become more active
 
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