When we think of the relationship between diet and osteoporosis, the first thought tends to be the impact of calcium and vitamin D.  While those are important, the relationship between diet and the disease is more complex.  Recent research has found that, in adolescents, food quality is highly impactful on bone health.

The risk of osteoporosis at 50 years of age and beyond is related to bone density developed during childhood and early adulthood.  The greater bone density is during that period, the lower the impact will be of the bone density loss in middle age.  Bone density typically declines 1-2% each year between ages 40 and 55 years.  This will represent a decline in bone density of 15-30% from the level present in early adulthood.  Those starting with higher bone density arrive at 55 years with greater bone density.

Getting back to early life diet, eating higher amounts of ultra processed foods (UPFs), now appears to govern early adulthood bone density.  UPFs are highly modified products created through industrial processes. They typically contain multiple additives, preservatives, and artificial ingredients. These foods, built for long shelf lives, include sugar-sweetened beverages, highly processed meat products, flavored yogurts, packaged snacks, and breakfast cereals.  Perhaps the most significant indicator of a UPF is the added sugar.

A whole, unprocessed diet containing 40% carbohydrate supplies approximately 30-35 grams of sugar.  The current intake in the standard American diet which contains a significant volume of UPFs is about 200 grams of sugar, or about 6-7 times that of a whole food, unprocessed diet.  This added sugar is there for one purpose, to drive taste preference which tends to increase consumption.

In the United States, UPFs are estimated to provide 58% of caloric energy.  US National Health and Nutrition Examination Survey data showed that from 1999 to 2018, the percentage of total energy consumption from UPFs increased from 61.4% to 67% in people aged 2-19 years.  This high intake of UPFs has been associated with increased risk of diabetes, fatty liver disease, cardiovascular disease and inflammatory bowel disease.  We now have to add osteoporosis to that list.

Bone must constantly be repaired removing areas with microcracks from use and filled back in with new bone.  The job of building this new bone is done by bone cells called osteoblasts.  These cells only live about 100 days and must constantly be replenished by mesenchymal stem cells (MSCs) from bone marrow.  This is where the negative impact of too much sugar comes in.  MSCs require NAD+ in significant amounts for their energy production and function.  Unfortunately, high sugar consumption depletes NAD+ robbing MSCs from this essential energy source needed to mature into osteoblasts in mice.(1)  Without enough NAD+, MSCs differentiate into fat cells rather than osteoblasts.

I had to include this image from the study which seems to highlight the problem.  Notice the mouse at the bottom of the image showing this shunting of MSCs away from bone cells and towards becoming fat cells.  I can’t tell which fast-food establishment the mouse got the drink from, but I think you get the message.

We will gradually lose bone density from middle life on with the rate accelerating from age 50 on.  Whether this becomes osteopenia, osteoporosis or remains healthy bone depends on what bone density one starts adulthood with.  What bone density one starts adulthood with depends on the amount of UPFs, particularly the sugars consumed up until that point.

By now the adults who have life prior to age 30 behind them the concept here is still highly relevant.  We must continue to regenerate bone throughout life.  While it is optimal to have that process as good as is possible in early life, it still helps to improve that outcome at any point.  A side effect – you will reduce the risk of a bunch of other chronic diseases.

1. Yen et al.  EXCESS GLUCOSE ALONE DEPRESS YOUNG MESENCHYMAL STROMAL/STEM CELL OSTEOGENESIS AND MITOCHANDRIA ACTIVITY WITHIN HOURS/DAYS VIA NAD + /SIRT1 AXIS.  Journal of Biomedical Science, 2024;31:49.