Bone loss happens when your body breaks down old bone faster than it can build new bone. This imbalance is universal after a certain age: both men and women lose about 3% of bone mass per decade starting around age 40. For women, the rate triples to roughly 9% per decade between ages 45 and 75 because of the additional loss triggered by menopause. Understanding why this happens, and what accelerates it, starts with how your bones constantly rebuild themselves.
How Your Bones Rebuild and Break Down
Bone is living tissue in a constant state of renovation. Two types of cells run the process. One type, called osteoclasts, attaches to the bone surface and dissolves it using acids and enzymes, leaving small scooped-out pits. Then a second type, called osteoblasts, moves in to fill those pits with fresh collagen and minerals. This cycle of tear-down and rebuild happens continuously from before birth until death.
In healthy younger adults, the two sides stay roughly balanced. Bone loss occurs when the demolition crew outpaces the construction crew. This can happen because osteoclasts become overactive, because osteoblasts slow down, or both. Nearly every cause of bone loss traces back to something that tips this balance.
Estrogen, Menopause, and Hormonal Shifts
Estrogen is one of the strongest regulators of bone turnover. It acts as a brake on osteoclast activity, keeping bone breakdown in check. When estrogen levels drop, that brake releases and bone resorption accelerates sharply. This is why menopause is the single largest driver of bone loss in women: you can lose up to 20% of your bone density within five years of menopause starting.
Men aren’t immune. Estrogen-deficient men experience the same accelerated bone turnover. Testosterone also plays a protective role, so men with low testosterone levels face a similar, though typically slower, decline. Other hormonal conditions contribute too. An overactive parathyroid gland (hyperparathyroidism) is the most common cause of high calcium in the blood, and it works by pulling calcium directly from bone, increasing the risk of both spinal and non-spinal fractures.
Not Enough Calcium or Vitamin D
Your body needs calcium for dozens of critical functions, from muscle contraction to nerve signaling. When you don’t get enough from food, your parathyroid glands release a hormone that essentially mines your skeleton for it. Over time, this steady withdrawal weakens bones from the inside out.
Vitamin D is the gatekeeper for calcium absorption in the gut. Without adequate vitamin D, even a calcium-rich diet won’t fully protect your bones because you simply can’t absorb enough. The current recommended intake for vitamin D is 600 IU per day for adults up to age 70 and 800 IU per day after 70. Many people fall short, particularly those who live in northern climates or spend most of their time indoors.
Medications That Weaken Bone
Glucocorticoids, commonly prescribed as prednisone or prednisolone for inflammation and autoimmune conditions, are the most well-known bone-damaging medications. Between 30% and 50% of people who take them long-term develop osteoporosis. The damage starts fast: bone strength drops measurably within the first three to six months of use, driven by a surge in osteoclast activity.
What surprises many people is how low the threshold is. Even doses as small as 2.5 to 7.5 mg of prednisolone per day raise vertebral fracture risk to more than two and a half times normal. At 7.5 mg or higher, fracture risk jumps to more than five times normal. Long-term use is defined as just three months of consecutive treatment, and roughly 1% of the adult population worldwide meets that threshold. If you take glucocorticoids regularly, bone health monitoring is worth discussing with your provider.
Other medications linked to bone loss include certain seizure drugs, some cancer treatments (particularly those that suppress sex hormones), and proton pump inhibitors used for acid reflux when taken for years at a time.
Chronic Diseases and Malabsorption
Several chronic conditions cause bone loss indirectly by interfering with nutrient absorption. Celiac disease is a prime example. The autoimmune reaction damages the lining of the small intestine, reducing the body’s ability to absorb calcium and vitamin D. About 25% of people with celiac disease develop secondary hyperparathyroidism as a result, where the parathyroid glands ramp up activity to compensate for low calcium, accelerating bone breakdown in the process.
Inflammatory bowel disease, chronic kidney disease, and rheumatoid arthritis all carry elevated bone loss risk through similar pathways: chronic inflammation, impaired absorption, or both. Type 1 diabetes and hyperthyroidism also contribute. In many of these cases, bone loss goes unnoticed until a fracture occurs because the underlying condition dominates medical attention.
Smoking, Alcohol, and Sedentary Living
Nicotine directly inhibits the formation of new bone and impairs blood vessel growth in bone tissue. It also alters parathyroid hormone levels and increases oxidative stress, creating multiple pathways to bone damage. The effect is dose-dependent: the more you smoke, the greater the loss.
Alcohol has a more nuanced relationship with bone. Up to about two drinks per day, no significant increase in fracture risk has been observed. Above that level, hip fracture risk rises substantially. Heavy drinking suppresses osteoblast function and interferes with calcium balance.
Physical inactivity may be the most underappreciated risk factor. Bone responds to mechanical stress by getting stronger, a principle called Wolff’s law. Without regular loading, there’s less stimulus for osteoblasts to build. Research comparing athletes to inactive individuals shows that regular vigorous weight-bearing exercise of one hour or more per week is associated with meaningfully higher bone density. A study of female athletes found that tennis players had 12% greater bone density in the spine than runners, and their dominant playing arm was denser than their non-dominant arm. The skeleton literally builds bone where it’s needed most.
Age-Related Decline
Even without any of the risk factors above, aging itself causes bone loss. The number of osteoblasts available to rebuild bone gradually decreases with age, while resorption continues at a steady pace. This slow-motion deficit compounds over decades. The 3% per decade loss that begins at 40 is a baseline that applies to both sexes, with menopause layering additional loss on top for women.
Peak bone mass, the maximum amount of bone you’ll ever have, is typically reached by the late 20s to early 30s. Everything after that is management. People who build more bone during adolescence and early adulthood enter middle age with a larger reserve, which is one reason childhood nutrition and physical activity have lifelong consequences for bone health.
How Bone Loss Is Measured
Bone density is assessed using a painless scan called a DEXA, which produces a T-score. A T-score of negative 1 or higher is considered healthy. Between negative 1 and negative 2.5 indicates osteopenia, a moderate thinning that signals increased risk. A T-score of negative 2.5 or lower is the threshold for osteoporosis. These numbers compare your bone density to that of a healthy 30-year-old, so some decline with age is expected, but the T-score tells you whether you’ve crossed into a range where fracture risk is significantly elevated.
Screening is typically recommended for all women at age 65 and for younger women and men who have risk factors like glucocorticoid use, smoking, low body weight, or a family history of fractures. The scan takes about 10 to 15 minutes and involves very low radiation exposure.