A small (57 g) daily portion of Jarlsberg cheese may help to stave off bone thinning (osteopenia/osteoporosis) without boosting harmful low density cholesterol, suggest the results of a small comparative clinical trial, published in the open access journal BMJ Nutrition Prevention & Health.
The effects seem to be specific to this type of cheese, the findings indicate.
Jarlsberg is a mild and semi-soft, nutty-flavored cheese made from cow’s milk, with regular holes. It originates from Jarlsberg in eastern Norway.
Previous research indicates that it may help boost levels of osteocalcin, a hormone that is associated with strong bones and teeth, but it’s not clear if this effect is specific to Jarlsberg or any type of cheese.
In a bid to find out, the researchers studied 66 healthy women (average age 33; average BMI of 24) who were randomly allocated to adding either a daily 57 g portion of Jarlsberg (41) or 50 g of Camembert cheese (25) to their diet for 6 weeks.
At the end of this period, the group eating Camembert was switched to Jarlsberg for another six weeks.
Jarlsberg and Camembert have similar fat and protein contents, but unlike Camembert, Jarlsberg is rich in vitamin K2, also known as menaquinone (MK), of which there are several varieties.
The short-chained MK-4 is found in animal products such as liver. The long-chained MK-7, MK-8, MK-9 and MK-9(4H) originate from bacteria, and occur in certain fermented foods, such as cheese. Jarlsberg is particularly rich in both MK-9 and MK-9(4H).
Every six weeks blood samples were taken from all the participants to check for key proteins, osteocalcin, and a peptide (PINP) involved in bone turnover. Vitamin K2 and blood fat levels were also measured.
Blood sample analysis showed that the key biochemical markers of bone turnover, including osteocalcin, and vitamin K2 increased significantly after 6 weeks in the Jarlsberg group.
Among those in the Camembert group, levels of PINP remained unchanged while those of the other biochemical markers fell slightly. But they increased significantly after switching to Jarlsberg. PINP levels also increased.
Glycated hemoglobin (HbA1c)-the amount of glucose stuck in red blood cells – fell significantly (by 3%) in the Jarlsberg group, while it rose sharply (by 2%) in those eating Camembert. But after switching to Jarlsberg HbA1c fell significantly in this group too.
Calcium and magnesium fell significantly in the Jarlsberg group but remained unchanged in the Camembert group. After switching cheese, calcium levels dropped in this group too, possibly reflecting increased uptake of these key minerals in bone formation, say the researchers.
“Daily Jarlsberg cheese consumption has a positive effect on osteocalcin, other [markers of bone turnover], glycated hemoglobin and lipids,” write the researchers, concluding that the effects are specific to this cheese.
The bacteria (Proprionebacterium freudenreichii) in Jarlsberg that produces MK-9-(4H) also produces a substance called DHNA, which, experimental studies suggest, might combat bone thinning and increase bone tissue formation, and possibly explain the increase in osteocalcin, they add.
They go on to suggest that Jarlsberg cheese might therefore help to prevent osteopenia—the stage before osteoporosis—as well as metabolic diseases, such as diabetes, although further research would be needed to confirm this, they emphasize.
“This study shows that while calcium and vitamin D are known to be extremely important for bone health, there are other key factors at play, such as vitamin K2, which is perhaps not as well known,” comments Professor Sumantra Ray, Executive Director, NNEdPro Global Centre for Nutrition and Health, which co-owns the journal.
The study also highlights an important research issue, he adds: “Different methods of preparation mean there are key differences in the nutrient composition of cheese which has often been regarded as a homogenous food item in dietary research to date. This needs to be addressed in future studies.”
But he cautions, “As this is a small study in young and healthy people designed to explore novel pathways linking diet and bone health, the results need to be interpreted with great caution as the study participants will not necessarily be representative of other groups. And it shouldn’t be taken as a recommendation to eat a particular type of cheese.”
Osteoporosis (OP) is the most common bone disease that affects elderly men and women . It is a metabolic skeletal disorder caused by an imbalance between bone formation and resorption, leading to a loss of bone mass and quality, skeletal structure deterioration and an increased risk of fractures [2,3]. OP is classified into a primary and secondary form with distinct etiological backgrounds. Type 1 (primary) is typical of postmenopausal women in whom the decrease in estrogenic levels is associated with an inflammatory state linked to an increase in osteoclast activity and a consequent imbalance of bone metabolism, whereas type 2 (secondary) occurs in both males and females, but its pathologic mechanism has only partially been clarified .
Vascular calcification (VC) is defined as the ectopic deposition of mineral matrix in the vessel wall. It occurs prevalently in aging and primary chronic conditions (hypertension, diabetes mellitus and chronic kidney disease), representing an important risk factor for cardiovascular morbidity and mortality [5,6,7,8]. Previously, the calcification of the vessel wall was known as a passive, degenerative and uncontrolled process caused only by the abnormal precipitation of calcium crystal in the vasculature [9,10]. Nowadays, a growing body of evidence suggests that it is an active, regulated event that shares similar characteristics with bone formation and metabolism. In particular, its discovery in the calcified vessel of bone-related proteins, bone-like structures and osteoblastic like-cells derived from vascular smooth muscle cells (VSMCs) has highlighted the active and cell-mediated nature of this vascular process [11,12,13,14,15,16].
Although OP and VC produce differing pathophysiological effects, their onsets frequently coexist in aging, representing one of the main public health problems with significant morbidity and mortality .
For many years, their coexistence was considered independent and only related to age , but several studies have provided support for a close link between bone and vascular health (Table 1) [19,20].
Clinical evidence linking bone loss to vascular calcification.
|Study||Name of the Study||Number of Patients Enrolled||Key Findings|
|||Framingham Heart Study||364 women and 190 men|
(28–62 years old)
|Bone loss was associated with progression of aortic calcification in women over 25 years|
|||Women’s Health Across the Nation Study||90 women|
(45–58 years old)
|Lower BMD was related to high aortic calcification|
|||MESA Study||946 women|
(mean age 65.5 years old)
and 963 men
(mean age 64.1 years old)
|Lower BMD was associated with greater coronary artery and abdominal aortic calcium score|
|||Rotterdam Study||582 men and 694 women|
all >55 years old
|BMD loss was significantly associated with higher follow-up coronary artery calcification|
In this regard, many findings suggest that bone loss in OP may promote and increase the risk of cardiovascular events and vascular atherosclerosis. In the Framingham, Women’s Health Across the Nation (SWAN), Multi-Ethnic Study of Atherosclerosis (MESA) and Rotterdam studies, loss of bone mineral density (BMD) was associated with the development and progression of aortic calcification as well as with a higher risk of cardiovascular disease (CVD) mortality [21,22,23,24,25,26,27]. On the other hand, a direct correlation between VC and risk of bone fracture was also found. The MINOS study, for example, emphasized that men with aortic calcification present a major risk of bone fracture . This was also found in healthy post-menopausal women with aortic calcification associated with lower BMD and increased risk of femur fractures (2.3-fold increase) .
Different hypotheses have been proposed to better explain the link between bone and vascular system, which is commonly referred to as “bone-vascular crosstalk”.
First, bone loss and vascular calcification share common risk factors, including smoking, physical activity, alcohol intake, Type 2 diabetes, menopause and hypertension. In addition, both are characterized by chronic low-grade inflammation and oxidative stress and by the involvement of bone morphogenetic proteins (BMP), osteoprotegerin, and parathyroid hormone, thus also suggesting common pathophysiologic mechanisms .
In this context, it is important to mention the role of the VitK2 family, lipid soluble compounds that play a pivotal role in the maintenance of calcium homeostasis . Specifically, it is involved in the “calcium paradox”, a phenomenon in which a low calcium deposition in the bone tends to be associated with a parallel increase of calcium deposition in the vessel wall as a consequence of impaired calcium metabolism [31,32,33].
Given that the role of VitK2 in bone-vascular crosstalk and the “calcium paradox” has only been partially explained, this review aims to describe and summarize the most relevant knowledge concerning the nature of this vitamin, its molecular mechanism and clinical outcomes at bone and vascular level.
reference link https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8067793/
More information: Effect on bone anabolic markers of daily cheese intake with and without vitamin K2: a randomised clinical trial, BMJ Nutrition Prevention & Health (2022). DOI: 10.1135/bmjnph-2022-000424