Examples of anti-inflammatory substances include the Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), such as aspirin, ibuprofen, and naproxen, and other substances like EPA and DHA from fish oil.

Anti-inflammatory drugs reduce age-related decreases in brain volume in cognitively normal older adults.

Neurobiol Aging. 2009 Apr 20. PMID: 19386384

Walther K, Bendlin BB, Glisky EL, Trouard TP, Lisse JR, Posever JO, Ryan L.
Cognition and Neuroimaging Laboratories, Department of Psychology, University of Arizona, Tucson, AZ, 85721, USA.

Previous studies have indicated a decreased risk for developing Alzheimer’s disease in anti-inflammatory (AI) drug users. Yet few studies have determined whether AI drug use provides a protective effect against normal age-related changes in the brains of older adults. Regional volume changes in gray and white matter were assessed cross-sectionally using optimized voxel-based morphometry in 36 females taking AI drugs as arthritis or pain medication and 36 age- and education-matched female controls. Although mean gray and white matter volume differences between AI drug users and the non-AI group were small, AI drug use interacted with age, such that the non-AI group showed significantly greater age-related volume changes in regions of both gray and white matter compared to the AI drug users. These regions included the superior and medial frontal gyri, middle and inferior temporal gyri, fusiform and parahippocampal gyri, and occipital gray matter as well as temporal, parietal, and midbrain white matter. The results are consistent with the notion that AI drugs provide protection against age-related changes in brain volume. It is possible that inflammation plays a role in volume decreases associated with normal aging, and that suppressing the inflammatory response moderates this decrease.

This is because, while the ability to degrade the matrix is extremely important in growth and wound healing, if the processes of synthesis and degradation fall out of balance in favour of degradation, the overall amount of collagen will decrease.

In youth, these processes are in balance, but as we age, the degradative enzyme activity begins to overpower that of synthesis, leading to a loss of skin quality. Other factors that increase MMPs are photodamage and smoking.

In the past, I’ve boosted my skin’s balance in favour of collagen synthesis with isotretinoin, which worked beautifully but has drawbacks that in my opinion make it unacceptable for chronic use (cracking lips, sun sensitivity, etc.). I’ve also heard that the skin’s response to collagen-synthesis stimulating retinoids decreases with age.

So, in theory, one could boost its overall levels by instead interfering with the breakdown of collagen by inhibiting MMPs.

At present, the only MMP inhibitor that’s available readily and cheaply is doxycycline hyclate, an antibiotic often used to combat acne. Apparently, by taking a subantimicrobial dose (i.e., too little to kill bacteria) one can benefit from its anti-MMP activity while minimizing its side effects. Doxycycline is also used in this way in dentistry, where it is used to facilitate healing of the connective tissue in the gums.

There was also a study where doxycycline’s effect on wound healing was investigated because it was suspected it may *interfere* with normal wound healing as a side-effect, but it was instead found that the wounds actually healed either at the same rate or faster.

So, lately I’ve been noticing the accumulation with age and decades of intense sunlight a slight loss of skin elasticity (yes, wrinkles), so I decided to start taking 25mg/day doxycycline for a couple of months and see if this has any effect on the quality of my skin. I’ve taken some ‘before’ photos that highlight the problem, and I intend to compare these with pictures taken in 1 and 2 months to see if I can identify any change.

The literature is at first glance almost entirely free of this kind of experiment, with most papers focussing on doxycycline’s antibacterial and anti-inflammatory effects for the treatment of acne and rosacea. I’m sure there’s a good reason for this that I in my limited capacity don’t have time to dig up, so I’m pressing ahead regardless.

I’ll post the results, including before/after shots and analysis in about a month

Here’s some reading in the meantime:

• Inhibition of matrix metalloproteinases: a new skin care frontier
• Matrix metalloproteinases
• Doxycycline

This is good news for lovers of ginger, such as myself. Cheers!

Ginger extract (Zingiber officinale) has anti-cancer and anti-inflammatory effects on ethionine-induced hepatoma rats.

Clinics. 2008 Dec;63(6):807-13. PMID: 19061005

Habib SH, Makpol S, Hamid NA, Das S, Ngah WZ, Yusof YA.

Department of Biochemistry, Medical Centre, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur.

OBJECTIVE: To evaluate the effect of ginger extract on the expression of NFkappaB and TNF-alpha in liver cancer-induced rats. METHODS: Male Wistar rats were randomly divided into 5 groups based on diet: i) control (given normal rat chow), ii) olive oil, iii) ginger extract (100mg/kg body weight), iv) choline-deficient diet + 0.1% ethionine to induce liver cancer and v) choline-deficient diet + ginger extract (100mg/kg body weight). Tissue samples obtained at eight weeks were fixed with formalin and embedded in paraffin wax, followed by immunohistochemistry staining for NFkappaB and TNF-alpha. RESULTS: The expression of NFkappaB was detected in the choline-deficient diet group, with 88.3 +/- 1.83% of samples showing positive staining, while in the choline-deficient diet supplemented with ginger group, the expression of NFkappaB was significantly reduced, to 32.35 +/- 1.34% (p<0.05). In the choline-deficient diet group, 83.3 +/- 4.52% of samples showed positive staining of TNF-alpha, which was significantly reduced to 7.94 +/- 1.32% (p<0.05) when treated with ginger. There was a significant correlation demonstrated between NFkappaB and TNF-alpha in the choline-deficient diet group but not in the choline-deficient diet treated with ginger extract group. CONCLUSION: In conclusion, ginger extract significantly reduced the elevated expression of NFkappaB and TNF-alpha in rats with liver cancer. Ginger may act as an anti-cancer and anti-inflammatory agent by inactivating NFkappaB through the suppression of the pro-inflammatory TNF-alpha.