Bone & Muscle Hub

The evidence behind DRV+

Bone, Muscle & Joint Health

Bone health: aware of the risk, not taking action

Our survey of 343 women, most peri- or postmenopausal, reveals a striking gap between how aware and concerned women are about bone health and how few take the steps that actually protect it.

343 respondents

2024–2025

Cross-sectional online survey

88% aware of the risk

42% rarely do protective exercise

68% want new support

Study Findings

We surveyed 343 women, most in midlife, on their awareness of and concern about bone health, the protective steps they take, their recognition of the gut–bone link, and the symptoms they already have.

What we found:

88.2% were aware of the postmenopausal risk to bone health and 77.2% were concerned - yet 42% rarely or never do weight-bearing or resistance exercise, the most protective behaviour, and this held even among those who were aware or concerned. Musculoskeletal symptoms were already common (78.7%, led by joint pain at 66.5%), the gut–bone link was under-recognised (43.3% didn't make the connection); and despite high concern, 41.1% were taking nothing for their bones, while 67.9% wanted a new solution.

What This Means

Awareness isn't translating into action

42% rarely or never do the exercise that protects bone density.

The gap holds even among women who are aware of the risk and concerned about it.

The gut–bone link is missed

43.3% don't recognise gut health as important for their bones.

Despite the gut's role in absorbing bone-critical nutrients like calcium and vitamin D.

A clear unmet need

41.1% take nothing for their bones, yet 67.9% want a new solution.

High concern with low action points to real demand for accessible, evidence-based support.

Read the abstract

Bone health, structure, cells and function

Bone Composition

Organic matrix (35%): Mostly type I collagen (provides tensile strength) and non-collagenous proteins like osteocalcin.

Inorganic matrix (65%): Mostly hydroxyapatite crystals (calcium phosphate), providing rigidity and strength.

Bone is dynamic: Constantly remodelling in response to mechanical stress, hormones and nutritional status.

Internal structure of a bone

Osteoblast

Origin: Mesenchymal stem cells.
Function: Build bone by synthesising collagen and promoting mineralisation. Eventually become osteocytes or undergo apoptosis.

Osteocyte

Origin: Former osteoblasts embedded in bone matrix.
Function: Regulate bone remodelling, sense mechanical stress and maintain calcium homeostasis.

Osteoclast

Origin: Haematopoietic stem cells (monocyte lineage).
Function: Resorb bone by secreting acid and proteolytic enzymes. Essential for bone turnover and calcium release.

Bone remodelling

Coupled process

Bone resorption by osteoclasts followed by bone formation by osteoblasts.

Regulated by

Mechanical stress: Load-bearing stimulates bone formation.

Hormones

PTH: Increases osteoclast activity (indirectly via RANKL).
Vitamin D: Promotes calcium absorption and bone mineralisation.
Oestrogen: Inhibits osteoclasts and promotes bone formation.
Calcitonin: Inhibits osteoclasts (less significant in adults).

Cytokines and signalling pathways

RANK/RANKL/OPG pathways. Wnt/B-catenin signalling for osteoblast activity.

Diagnosis

Bone Mineral Density (BMD): via DXA scan is the gold standard. T-score ≤ –2.5 at the femoral neck or spine confirms osteoporosis.
FRAX Tool: Estimates 10-year probability of hip and major osteoporotic fractures, incorporating clinical risk factors with or without BMD.

Muscle health, physiology and structure

Types of muscles

Control

Location

Function

Skeletal

Voluntary

Attached to bones

Movement, posture

Smooth

Involuntary

Vessels, bladder

Peristalsis, vasoregulation

Cardiac

Involuntary

Heart

Pumping blood

Skeletal

Control Voluntary

Location Attached to bones

Function Movement, posture

Smooth

Control Involuntary

Location Vessels, bladder

Function Peristalsis, vasoregulation

Cardiac

Control Involuntary

Location Heart

Function Pumping blood

Skeletal muscle structure

Muscle fibre: Multinucleated cell composed of myofibrils

Myofibrils: Repeating sarcomeres (basic contractile unit).

Sarcomere: Actin (thin) and myosin (thick) filaments that slide for contraction (sliding filament theory).

Excitation-contraction coupling: Action potential Ca²+ release from sarcoplasmic reticulum → cross-bridge cycling contraction.

Muscle fibre types

Features

Metabolism

Fatigue

Resistance

I (Slow-twitch)

High Mitochondria

Myoglobin

Oxidative

High

IIa (Fast oxidative)

Intermediate

Both

Moderate

Walking

IIb (Fast glycolytic)

Low Mitochondria

Anaerobic Glycolysis

Low

Sprinting

I (Slow-twitch)

Features High Mitochondria

Metabolism Myoglobin

Fatigue Oxidative

Resistance High

IIa (Fast oxidative)

Features Intermediate

Metabolism Both

Fatigue Moderate

Resistance Walking

IIb (Fast glycolytic)

Features Low Mitochondria

Metabolism Anaerobic Glycolysis

Fatigue Low

Resistance Sprinting

The physiology of muscle protein synthesis

Skeletal muscle is in a constant state of protein turnover - the balance between muscle protein synthesis and muscle protein breakdown. Net positive balance leads to hypertrophy; net negative balance results in atrophy.

Dietary protein provides essential amino acids, particularly leucine, which is a potent stimulator of the mechanistic target of rapamycin complex 1 pathway - an intracellular regulator of muscle protein synthesis.(1) Postprandial muscle protein synthesis is maximally stimulated by ~20–30g of high-quality protein providing ~2–3g of leucine.(2)

Sarcopaenia and cachexia

In ageing, chronic illness, or disuse, protein intake becomes critical in preventing muscle catabolism.³

Sarcopaenia: Associated with reduced appetite, digestion and muscle anabolic response.
Cachexia: An inflammatory state (e.g. in cancer or COPD) elevates protein requirements.

Protein supplementation can help maintain lean body mass, reduce frailty, improve mobility and function, and improve hospital-related muscle loss.

Quality of protein: PDCAAS and DIAAS: PDCAAS (Protein Digestibility-Corrected Amino Acid Score) and the more modern DIAAS (Digestible Indispensable Amino Acid Score) quantify protein quality. Animal proteins typically score >1.0; plant proteins are variable, but a combination of plant proteins, found in DRV Protein & Creatine Super Blend, are combined to meet needs.⁴

Plant-based proteins: Plant proteins are gaining attention for their sustainability, digestibility and bioactive compounds. Plant-based proteins can support muscle protein synthesis if: dosed appropriately, combined strategically and optimised for leucine content.

Muscle-bone interaction

Mechanical loading

from muscle contraction stimulates bone growth (myokine–osteokine crosstalk).

Muscle wasting

(sarcopenia) and bone loss (osteopenia/osteoporosis) are interconnected, especially in ageing.

Myokines (e.g. irisin, IL-6)

Secreted by muscle, influence bone metabolism.

Osteokines (e.g. osteocalcin)

Secreted by bone, affect muscle function.

Clinical Considerations

Osteoporosis

Loss of bone mass and microarchitectural deterioration.
Common in postmenopausal women and the elderly. DXA scan to assess BMD (T-score ≤ -2.5 = osteoporosis).
Risk factors: low oestrogen, immobility, corticosteroids, vitamin D deficiency, smoking and poor diet.

Sarcopaenia

Age-related loss of muscle mass, strength and function.
Increases falls, fractures, morbidity.
Diagnosed via grip strength, gait speed and muscle mass (DXA/BIA).

Osteosarcopaenia

Concurrent loss of bone and muscle.
Shared risk factors: ageing, inactivity, malnutrition, chronic inflammation.
Interventions target both systems simultaneously.

Osteporosis

Osteoporosis is a systemic skeletal disorder that causes reduced bone mass and microarchitectural deterioration of bone tissue, leading to increased bone fragility and fracture risk. It remains underdiagnosed and undertreated, despite being a major contributor to morbidity in ageing populations, especially postmenopausal women and older men.

Stages of osteoporosis

Epidemiology

Globally, osteoporosis affects approximately 200 million women, with 1 in 3 women and 1 in 5 men over 50 expected to experience an osteoporotic fracture in their lifetime. The most common fracture sites include the hip, spine and wrist. Hip fractures in particular are associated with significant mortality and functional decline.

Pathophysiology

Bone remodelling is a continuous process involving osteoclast-mediated resorption and osteoblast-mediated formation. In osteoporosis, the balance shifts towards resorption. In women, oestrogen deficiency post-menopause accelerates bone loss. In men, age-related decline in testosterone and secondary causes (e.g. corticosteroid use, hypogonadism) are often contributory.

Risk Factors

Non-modifiable: Age >50, female sex, Caucasian or Asian ethnicity, family history of osteoporosis or fragility fracture.
Modifiable: Sedentary lifestyle, smoking, excessive alcohol, low calcium/vitamin D intake, low body weight or BMI <18.5, certain medications (e.g. glucocorticoids, PPIs, anticonvulsants), and secondary medical conditions (e.g. RA, hyperthyroidism, malabsorption syndromes).