So I was reading the latest book by Tim Ferriss the other day and Tim asks Lewis Cantley, a professor at the University of Harvard that has authored over 400 research paper, what he would put on a billboard. The guy said: “Sugar is toxic”. He then went on to explain how bad sugar is and included fruit in his argument and said some stuff in the lines of – fruit, when eaten in excess converts to fat and that creates insulin resistance, obesity, disease, etc.
And I looked up to my wife who was also sitting with me in the living room and I was like: “Babe, you won’t believe what I just read.”
I went on a rant and tangent for like 10 minutes about what this guy was saying and how wrong he was and I can’t believe he has a PhD and spews such nonsense. I knew I was preaching to the choir but I was so upset about this.
And then she was like: “What the fruit!”
We had a good laugh and that sparked the motivation for this article, which is long overdue in any way, so I hope you enjoy and learn that sugar and fruits are not bad or fattening or promotes disease.
As a side note, I do know there are a lot of other people that also think sugar is toxic, such as Dr Robert Lustig, but when I read that from the book, it really motivated me to write this.
Sugar or sucrose consists of fructose and glucose molecules. The sucrase enzyme in the gut breaks the bond and the free glucose and fructose are then absorbed.
Fruits also contain fructose and glucose and the ratio differs between the different fruits. High fructose fruits include apples, pears, mangoes, etc., and some low fructose fruits include honeydew melon, cantaloupe, bananas, blueberries, strawberries, etc.
Some quick facts about the difference between fructose and glucose:
- Fructose is slowly absorbed and delays gastric emptying, whereas glucose is rapidly absorbed. Fructose enters the epithelial intestinal cells via the GLUT5 transporter by the mechanism of facilitated diffusion, whereas glucose enters the enterocytes via sodium-glucose-cotransporter 1, an active transporter.
- The liver takes up the majority of fructose after a meal but skeletal muscle, adipose tissue, and the kidney also contribute to fructose clearance from the blood. Glucose is taken up by the muscles and then lastly by the liver. Fructose uptake into cells are insulin-independent and glucose uptake is insulin dependent.
- Glucose is metabolized in the cell either to glycogen or to pyruvate by glycolysis. Fructose is converted to fructose-1-phosphate by fructolysis which consumes ATP, creating AMP. Fructose-1-phosphate can then also be converted to glycogen or pyruvate. Because fructose can enter cells uncontrollably and is converted to fructose-1-phosphate, an excess of fructose will deplete ATP and cause damage. In theory this might be a point against fructose, however, no studies in humans have proven this yet.
I want to address some concerns some people might have with fructose, sugar or fruit consumption, and its effect on triglycerides, uric acid and risk of gout, insulin resistance, weight gain and general health.
Fructose & triglycerides
Fructose is thought to be more lipogenic than glucose and will elevate triglycerides. However, stable isotope tracer studies have found that de novo lipogenesis pathway for fructose in humans is very minor (<1%) at moderate intake and up to 5% in the overfed state, which is very unlikely to happen from whole fruit consumption (R). Well, this study by Buul et al. showed that when 250g of fructose is given, less than 10% of the fructose load was converted to lipids after 6 hours, which means that less than 1g of fat is created per hour from a massive unnatural amount of fructose (R). Plus, hepatic and serum copper levels are inversely correlated with the severity of non-alcoholic fatty liver disease (NAFLD) (R) and when copper is deficient, people get fatty liver.
In this study (R), people were overfed, a 150% caloric surplus, with 300g of sugar a day. They were then either fed a high protein low-fat (HP-LF) diet (2.7g/kg/BW protein – 10% fat) or a low protein high-fat (LP-HF) diet (0.8g/kg/BW protein – 20% fat).
Fat in the liver (intrahepatocellular) increased from 25.0 to 147.1mmol/kg wet weight (ww) after LP-HF and from 30.3 to only 57.8 after HP-LF. Fat in the muscles (intramyocellular) increased from 7.1 to 8.8mmol/kg ww after LP-HF and from 6.2 to 6.9 after HP-LF. Massive difference. If the protein intake was even higher, lipids might not even have accumulated at all. That said, I’m not advising anyone to overfeed with a 50% surplus anyway, and especially not on 300g of refined sugar. If the study was done with fruit, the results would have been totally different as well.
A meta-analysis in 2018 showed that fructose consumption through fruit, in doses of 22.5 to 300g/day didn’t adversely affect glycaemic control, insulin sensitivity, postprandial lipids and markers of NAFLD (R).
Fructose & uric acid
Fructose is able to increases uric acid whereas glucose doesn’t. Uric acid is actually a very potent anti-oxidant in the body and protects the body against oxidative stress. Fruit consumption actually lowers uric acid (R) and this study found that fructose consumption doesn’t contribute to inflammation more than glucose (R).
A the same meta-analysis of 2018 with fructose consumption between 22.5 to 300g/day, they found that it also didn’t adversely affect uric acid concentrations in the body (R).
Fructose & Insulin sensitivity
Fructose, when co-ingested with glucose, as in the case of sucrose or fruit, increases glucose uptake into cells and significantly contributes to glycogen synthesis compared to glucose alone, which suggests that fructose contributes to the action of insulin.
Fructose has a GI of 19 and glucose of 100 making fructose, fruits and even sugar much less insulinogenic than glucose and starches.
There is evidence that small, ‘catalytic’ doses ( ≤ 10 g/meal) of fructose decrease the glycaemic response to high-glycaemic index meals in humans (R). Even dried fruits, such as dried apricots (GI = 42), raisins (GI = 55), sultanas (GI = 51), dried apples (GI = 43), dried jujubes (GI = 55), when ingested with white rice or white bread, which is very insulinogenic, were able to significantly reduce the glycemic response. Adding a bit of nut, such as almonds, lowers the glycemic response even more (R).
Another study shows that ≤50 g/day or ≤10% of total energy intake/day of fructose reduces Hb1Ac and fasting glucose (R). That is 4 large (900g) apples or 100g (6-7 tablespoons) of sugar.
A meta-analysis in 2017 (R) concluded this (emphasis mine):
“We included 14 comparison arms from 11 trials, including 277 patients. The studies varied in length from 2 to 10 wk (mean: 28 d) and included doses of fructose between 40 and 150 g/d (mean: 68 g/d). Fructose substitution in some subgroups resulted in significantly but only slightly lowered fasting blood glucose (-0.14 mmol/L; 95% CI: -0.24, -0.036 mmol/L), HbA1c [-10 g/L (95% CI: -12.90, -7.10 g/L; impaired glucose tolerance) and -6 g/L (95% CI: -8.47, -3.53 g/L; normoglycemia)], triglycerides (-0.08 mmol/L; 95% CI: -0.14, -0.02 mmol/L), and body weight (-1.40 kg; 95% CI: -2.07, -0.74 kg). There was no effect on fasting blood insulin or blood lipids. We included randomized controlled trials of isoenergetic replacement of glucose, sucrose, or both by fructose in adults or children with or without diabetes of ≥2 wk duration that measured fasting blood glucose.”
Fructose & Fat loss
High fruit, but not vegetable intake is inversely associated with the risk of becoming overweight or obese (R).
Fructose is very unique because it doesn’t require insulin to enter a cell. This allows fructose to boost the metabolism and energy expenditure and normalize the thermic response where glucose is unable to due to insulin resistance (R). The total increment in energy expenditure (EE) above baseline was similar with fructose (130 +/- 24 kJ/6 h) and sucrose (141 +/- 17 kJ/6 h), and is higher with sucrose than starch (108 +/- 24 kJ/6 h) and glucose (94 +/- 20 kJ/6 h). Sucrose also increases the metabolic rate to a greater extent than fructose or glucose alone (R).
When it comes to fat loss, this study found that a moderate (50–70 g/day)-fructose diet compared to a low- (<20 g/day) fructose diet, led to greater fat loss of 4.19kg vs 2.83kg over 6 weeks (R). Plus, consuming a high fructose high protein breakfast boosts diet-induced thermogenesis to a greater extent than a high protein high glucose breakfast (R). This shows that there is a synergistic effect between fructose and protein to boost fat loss. Add some MCT, caffeine and red pepper, and the thermic effect goes through the roof.
Another bonus for fructose is that it speeds up the oxidation of carbohydrates, by stimulating pyruvate dehydrogenase, to a greater extent than glucose and starch (R).
When it comes to sugar and fructose consumption, I don’t advise overeating on refined sources, but when it comes to fruit, there are only benefits.
The beneficial health effects of consuming dietary fiber from whole fruits include: improving gut health (positively modulating gut bacteria, reducing inflammation, improving diarrhea, constipation, IBS, IBD, Ulcerative Colitis, etc); lowering elevated LDL-cholesterol; reducing the risk of excessive weight gain and obesity; decreasing cardiovascular disease (CVD), coronary heart disease (CHD) and mortality risks; reducing risks of several cancers, stroke and type 2 diabetes; and improving the odds for successful aging.
Have you ever heard: “Oh, I ate too many apples and now I’m a diabetic with cardiovascular disease.”?
No. Instead you hear: “An apple a day keeps the doctor away.”
Don’t be afraid of fruit, but when eating foods in excess, such as calorie surplus, stick to whole fruits and reduce added sugar as much as possible. But when eating at maintenance or in a deficit, added sugar will not contribute to health problems.