35% TCA Peel of My Face and Neck

Day 5

About January 22, this year, I decided to do a 15% Jessner's peel on top of a 25% TCA peel on my face, neck, and décolletage.   I got the idea in my reading, and watching of Youtube videos on the subject.  Warning, this shouldn't be done without doing preliminary more superficial peels to determine one's tolerance.  

Let me say this about chemical peels.  It is possible to burn and even scar the skin, but it is not probable.  Why?  TCA and Jessner's peel are both self neutralizing, and will stop working after five or then minutes by themselves.  They also can be neutralized by washing with water.  Moreover, should the epidermis layer be breached, and you get down to the dermis, the water in the dermis will itself neutralize the chemical, so that deep burns will not happen.  

After a few weeks, I decided I wanted to try a 35% TCA peels for the first time.  This time I didn't put a Jessner's peel on first.  The purpose of doing this would be to prepare for the TCA peel.  I suppose I felt that it might be too much for a first attempt.  

I'm very happy with the way this peel turned out.  It may be that the two peels together made more of a difference.  I was reluctant to venture into doing this level of peel myself.  One should be experienced, but how could I get experience without doing the peel?  I had decided to go to a doctor's office for this, but they felt I had done all that could be accomplished with peels and I needed laser.  Maybe I should plan on four laser treatments.  While they said one treatment would cost $1100, they also wanted $900 for the anesthesia and $550 for "supplies."  They didn't want to do an aggressive peel, as this could cause burns.  OK, but I came there for an expert to do a more aggressive peel than I was comfortable with doing by myself.  But then, what peel have I ever been comfortable with?  They have all been ventures into the unknown.  

I bet anything I would not have been more satisfied with the results of the laser if I had gone that route.  What I accomplished is exactly what I set out to do.  I wanted to first and foremost get rid of the wrinkles on my lower eyelids.  Done!  :)). I wanted to tighten the skin as much as I could.  Done!  I wanted to get rid of hyper pigmentation, dark spots and growths.  Done!  

In the above photos, I direct your attention to some of the successes of this happy peel.  My under eye lids are nice and smooth, not wrinkly.  I was also surprised that wrinkles around my lips disappeared.  I had been trying to eliminate darkness on my upper lip, and I was thrilled at how beautifully they turned out. My skin tone is better than it's been since I was a teenager.  The elevens between my eyebrows are smoother.  My décolletage looks almost brand new.  Circles around my neck vanished.  Yay!  I didn't expect things to go as well as they did.  These photos are without makeup except lipstick and eyebrow tint.  

I could point out that my poor neck took a drubbing and isn't healed yet.  It will be OK in about a week.  I've been told to never, ever peel you neck.  When I was told this I had already peeled my neck without any trouble.  I don't think one should have a deep peel of the neck, but this wasn't a deep peel.  

I wish I had gone ahead and done my upper eyelids.  I have done them in the past.  The peel in January did not include upper or lower eyelids.  This peel I did lower eyelids but not upper.  Why?  I had gotten very aggressive with the bridge of my nose and the area between my eyebrows and then done my lower eyelids.  I actually realized suddenly that I felt faint!  What?  I gave myself a moment to recover, and the faintness passed, but I didn't think it was a good time to do my upper eyelids.  Some other day.  

I'm so happy with the way this has turned out for me.  Will I do this again soon?  Maybe.  Maybe not.  I still have a few growths and spots, especially on my nose.  I'd like to do my upper eyelids.  But after that I'll probably just go into maintenance mode.  

  

Followup on TCA 35% Peel on Hands and Forearms.

Day 5

This is Day 5 of my TCA 35% peel on my hands and forearms.  This is a work in process.  

Honestly, I may not do another TCA peel on my hands or arms.  Why?  Have I reached perfection?  No, but I just can't take another round like this one.  

The previous peel was 25%, but since I did two layers I suppose it amounted to about the same thing.  It was extremely itchy, to the point that it kept me awake.  That time the itchiness lasted for two days.  This time it lasted for four days.  I didn't use any Lidocaine or pain medicine except for Gold Bond cream.  The Lidocaine really keeps me awake.  

I put extra acid on some of the dark spots I'd like to peel off.  I haven't completely peeled yet, so my hand looks a little leathery.  

My wrist went wild with a rash.  It was so itchy that I scratched myself to pieces.  Of course, you're not supposed to do that.  

But, things are OK, despite slow progress.  Hands and arms peel slower than the face.  This rash was a lot worse a couple of days ago, so it's clearing up.  

So if I've decided not to do this again, does that mean I'm done with the beautification treatments on my hands and arms?  No!  I am planning to try other means.  Like what?  Oh, dry rubbing, micro needling, other types of peels, like Jessners.  Jessners has an anti inflammatory ingredient that I think would do better for me. 

What went wrong?  Well, I still think when the dust settles that my peel will turn out nicely.  It will probably take a couple of weeks more, maybe even three weeks, to see the results, because things heal more slowly in these areas.  I might think I had an allergic reaction, but I did my face and neck on the same day and didn't have the itching.  The area with the rash was an area that I burned on my other peel, so no doubt this skin is just damaged to start with.  

I burned my wrist because I had a scar that I treated aggressively with TCA, and I overdid it.  And it didn't improve the scar especially.  I think micro needling might do more for the scar.  And of course Retin A. 

I noticed three other areas of concern that I was trying to address with the peel.  Number one, I wanted to get rid of dark spots.  Some might call them age spots.  Well, they sure aren't youth spots.  I tried hydroquinone cream.  That was useless.  The peels have really been helpful for eliminating dark spots.  Number two, the skin texture was going south.  I had wrinkles and my arms had begun to  crepe and develop cellulite.   Number three, the skin on my arms was blotchy.  This was from sun damage.  

I did a Jessner's peel about six weeks ago on my left arm, and I was really pleased with the way the blotchiness went away.  The peel was so easy, causing no discomfort.  Then when it was healed, after about a month, I began to put castor oil on my hands and arms, and brush with a scalp shampoo brush, a nice soft one.  This removed the dead skin from the peel, and it has also just about gotten rid of the cellulite.  But does the skin still crepe?  I can't tell yet.  Maybe in a couple more weeks it will look OK.  

I did notice that the rings around my wrist/hand where they meet is much less wrinkly.  

I'll post again about this in about a month when the final results are in. 

Youtube threatens to ban Alex Jones

https://www.cnn.com/2018/02/23/us/infowars-youtube-videos-trnd/index.html



Am I a big fan of Alex Jones?  Oh, I suppose he's not my style.  Not that I'm anti Alex.  Just not that interested.  

But what's this??  Youtube has told Alex Jones that they will ban him if he gets two more strikes??  Oh, wait.  Youtube did that to me too.  Why?  I don't know.  I have hundreds of playlists on Youtube, and although Youtube seemed fine with whoever posted some video that I dare not have on my playlist, and their video, I was treading on the waters of being "banned for life" from Youtube.  THEY DELETED MY OFFENSIVE PLAYLIST!!!!!!  THERE!!!!  What was on my offensive playlist?  I don't have any idea.  It was titled "Jared."  

https://www.youtube.com/watch?v=kwMCIe2AGW8

(Link to Anderson Cooper/CIA)

Am I "far right," as CNN claims in their propaganda that Alex Jones is?  I am conservative.  This means number one, I am a Christian.  I am against lying, cheating, stealing, killing.  Pro life.  Am I racist?  Well, if that means living in the vicinity of the South and having a slight accent.   Otherwise no.  I don't like some people, like the lovely Nazis that run Youtube.   

So what in CNN's mind is far right about Alex Jones?  He has given credence to "conspiracy theories."  Oh????  What are conspiracy theories.  Conspiracy theories is a term coined by the KGB, oh, I mean the CIA, to undermine views counter to the official version of the assassination of President Kennedy.  

Was Anderson Cooper ever in the KGB/CIA?  Oh yeah.  That was a long time ago.  

What would end the terror reign of the CIA and all its alphabet soup minions?  Quit paying them.  

35% TCA Peel on my Hands and Forearms

https://www.parkercenter.net/gallery-patient/upper-eyelid-lift-patient-19/


This isn't me, and it isn't a photo of hands or arms.  It's a photo of a woman who had a Hetter's peel.   It's just remarkable to me the benefits that can come from a chemical peel.  

Today I decided to do a 35% TCA peel on my hands and forearms.  It's the first time I've ever used 35% TCA.  

I have peeled my hands and wrists in the past with 25% TCA, and I put a second layer on after five minutes.  That was too much, but I recovered.  

This time I put one layer of 35% TCA on my hands and arms, up to and including my elbows.  Why would I do such a thing?  I wanted to spruce up my hands, and I had blotchy skin on my arms due to sun damage.  Worst of all, I still had some dark spots that remained from the last peel, although much improved.   Of all the things I've done to get rid of those spots, this has by far been the best.  

I set up my area on the kitchen table, covering a space with towels. I put out a large bowl of water in case I wanted to rinse off the skin in a hurry.  Then I poured about 1/8th oz. of 35% TCA in a tiny bowl.  I washed my hands and arms with gel type hand soap, and then wiped my arms with nail polish remover, which is acetone.  This was to remove oil from the surface of my skin.  I used gloves, cotton gauze and cotton swabs to apply the peel.  

I did my hand left arm first, and checked the time.  At first I could hardly feel anything.  Then there was a stinging, but not as much as I thought there might be.  There were places where I even frosted, and then I saw that there were some places that I missed.  So I dabbed on more chemical peel on the areas I missed.  I put extra peel on the dark spots with a cotton swab.  Then I waited about twenty minutes.  That went OK.  I wanted to wait for the chemical to dry so I could put a glove on my left hand.  Then I did the same thing to my right hand and arm. 

It's been an hour and a half.  There was some stinging, but not intense.  I only did one layer because I have never tried 35% TCA before and I don't have a good idea of how much it will do.  I haven't washed it off yet, but I will in a few minutes.  

Stay tuned.  

More thoughts about K2

Vitamin K may play an important role in the prevention of fractures in postmenopausal women with osteoporosis. Menatetrenone is the brand name of a synthetic vitamin K2 that is chemically identical to menaquinone-4. The present review study aimed to clarify the effect of menatetrenone on the skeleton in postmenopausal women with osteoporosis, by reviewing the results of randomized controlled trials (RCTs) in the literature. RCTs that investigated the effect of menatetrenone on bone mineral density (BMD), measured by dual-energy X-ray absorptiometry and fracture incidence in postmenopausal women with osteoporosis, were identified by a PubMed search for literature published in English. Eight studies met the criteria for RCTs. Small RCTs showed that menatetrenone monotherapy decreased serum undercarboxylated osteocalcin (ucOC) concentrations, modestly increased lumbar spine BMD, and reduced the incidence of fractures (mainly vertebral fracture), and that combined alendronate and menatetrenone therapy enhanced the decrease in serum ucOC concentrations and further increased femoral neck BMD. This review of the literature revealed positive evidence for the effects of menatetrenone monotherapy on fracture incidence in postmenopausal women with osteoporosis. Further studies are required to clarify the efficacy of menatetrenone in combination with bisphosphonates against fractures in postmenopausal women with osteoporosis.

Keywords: vitamin K2, postmenopausal women, undercarboxylated osteocalcin, femoral neck, bone mineral density (BMD)

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Vitamin K₂ Therapy for Postmenopausal Osteoporosis

Jun Iwamoto

Author information ► Article notes ► Copyright and License information ►

This article has been cited by other articles in PMC.

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Vitamin K may play an important role in the prevention of fractures in postmenopausal women with

Abstract

1. Introduction

There are two types of naturally occurring forms of vitamin K, phylloquinone and menaquinones. All forms of vitamin K contain a 2-methyl-1,4-naphthoquinone ring as part of their structure, and individual forms differ in the length and degree of saturation of a variable aliphatic side chain attached at the 3-position (Figure 1). Phylloquinone (vitamin K1) is the major type of dietary vitamin K, while menaquinone-4 (vitamin K2) is the major form of vitamin K in the tissues, including bone. Vitamin K1 is supplied by the diet, especially in green leafy vegetables, while vitamin K2 is synthesized by bacteria in the gut. A number of foods also contain vitamin K2, notably natto(fermented soy beans), cheese, and curds, with natto being the richest source of vitamin K known.

Figure 1

Naturally occurring forms of vitamin K—Phylloquinone (vitamin K1) and menaquinones (vitamin K2).

Vitamin K is known to be a cofactor of γ-carboxylase, which converts three glutamic acid (Glu) residues in osteocalcin (OC) to γ-carboxyglutamic acid (Gla), and is thus essential for γ-carboxylation of OC [1,2,3,4]. Without this modification, OC becomes undercarboxylated OC (ucOC), which lacks structural integrity and the ability to bind to the mineral hydroxyapatite (Figure 2). The carboxylation reaction is completed as an intracellular posttranslational event, and secreted OC cannot longer be carboxylated. Impaired vitamin K nutritional status or warfarin use results in high concentrations of serum ucOC, resulting in an increased risk for fractures. In Japan, the cut-off values of serum ucOC concentrations for an increased risk for fractures associated are set at 4.5 ng/mL for treatment-naïve postmenopausal women and 2.6 ng/mL for postmenopausal women treated with amino-bisphosphonates [5,6]. Thus, vitamin K may play an important role in the prevention of fractures in postmenopausal women with osteoporosis.

Figure 2

γ-Carboxylation of osteocalcin by vitamin K.

Menatetrenone is the brand name of a synthetic vitamin K2 that is chemically identical to menaquinone-4. It is approved as an anti-osteoporotic medicine by the Ministry of Health, Labour, and Welfare in Japan. Menatetrenone is therefore a drug, rather than just a simple dietary supplement, and is used as an anti-osteoporotic medicine in Asia. The possible side effects are gastrointestinal tract symptoms such as discomfort of stomach and diarrhea, because vitamin K is a fat-soluble vitamin. The contraindication of menatetrenone is warfarin use, because vitamin K set off the anticoagulant effect of warfarin. Apart from this contraindication, menatetrenone (vitamin K2) does not cause any serious side effects regardless of its dose [7].

A dose-finding study of menatetrenone in Japan [7] administered daily doses of 15, 45, 90, and 135 mg and revealed that 45 mg was the minimum effective dose for improving bone mass parameters evaluated by microdensitometry and/or single photon absorptiometry in postmenopausal women with osteoporosis. This optimal dose (45 mg/day) for the treatment of osteoporosis is about 150–180 times greater than the recommended daily dietary intake of vitamin K (250–300 μg) [8]. No toxic effects of menatetrenone (45 mg/day) have been reported [7]. High-dose vitamin K is needed to prevent fractures in postmenopausal women with osteoporosis [9]. However, the effect of menatetrenone on the skeleton remains a matter of controversy [10,11,12,13,14,15,16,17], and the role of menatetrenone in the treatment of osteoporosis therefore needs to be clarified. In clinical practice, menatetrenone is frequently used in combination with bisphosphonates.

The objectives of the present study was to clarify the effects of menatetrenone on serum ucOC concentrations, bone mineral density (BMD), and fracture incidence in postmenopausal women with osteoporosis, by reviewing the results of randomized controlled trials (RCTs) in the literature.

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2. Approaches to Determining the Effect of Menatetrenone on Bone Health

RCTs that investigated the effect of menatetrenone on the skeleton of postmenopausal women with osteoporosis were identifiedby a PubMed search for literature published in English using combinations of terms “vitamin K2 or menatetrenone”, “bone”, “postmenopausal women”, and “osteoporosis”. The effects of menatetrenone on the skeleton were analyzed based on the data from the RCTs retrieved. The endpoints included BMD measured by dual-energy X-ray absorptiometry and fracture incidence. Eight studies met the criteria for RCTs on the effect of menatetrenone on the skeleton of postmenopausal women with osteoporosis [10,11,12,13,14,15,16,17]. Of eight RCTs, one included postmenopausal women with osteopenia or osteoporosis [15].

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3. Menatetrenone Monotherapy

Menatetrenone reduces serum ucOC concentrations [17,18]. The anti-fracture efficacy of menatetreone in postmenopausal osteoporosis has been shown in eight RCTs (Table 1) [10,11,12,13,14,15,16,17]. Of the eight RCTs, six were performed in Japan, one in Indonesia, and one in China. One Japanese RCT was a phase IV trial (Osteoporotic Fracture (OF) study) conducted in a large sample of postmenopausal women with osteoporosis (n = 4378) [13]. The dose of menatetrenone was 45 mg/day in all these studies. Placebo controls were used in one RCT, non-treatment controls in four RCTs, calcium supplementation controls in two RCTs, and active controls (alfacalcidol) in one RCT. The number of study subjects ranged from 44–4378 in the menatetrenone and control groups, and the study periods ranged from 1–3 years.

Table 1

Effects of menatetrenone on bone mineral density (BMD) and fracture incidence in postmenopausal women with osteoporosis: Randomized controlled trials.

Except for the OF study, RCTs with small sample sizes showed non-significant or modest effects on BMD of the lumbar spine and distal radius, and similarly low efficacy against fractures (mainly vertebral fractures) in postmenopausal women with osteoporosis (Table 1). A pivotal Japanese RCT conducted by Shiraki et al [10], showed that menatetrenone modestly increased lumbar spine BMD and reduced the incidence of clinical fractures in postmenopausal women with osteoporosis (relative risk: 0.45). A post-hoc analysis of the OF study showed a decrease in the incidence of vertebral fractures in postmenopausal women with a history of at least five vertebral fractures (relative risk: 0.61). There was an absence of a significant anti-fracture effect of menatetrenone in the subjects as a whole in the OF study [13]. The reason for this result was that many of the patients enrolled in the study might have had mild osteoporosis and a lower risk of developing fractures, probably because of the use of less specific diagnostic criteria for osteoporosis, which were only based on radiographic grading of bone atrophy and disregarded other risk factors for fractures [13].

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4. Combined Menatetrenone and Alendronate Therapy

Hirao et al. [19] conducted a RCT to examine the benefit of combined menatetrenone and alendronate therapy in postmenopausal women with osteoporosis. The increase in femoral neck BMD and the decrease in serum ucOC concentrations were greater in the alendronate plus menatetrenone group compared with the alendronate alone group.

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5. Discussion

Impaired vitamin K nutritional status impairs γ-carboxylation of OC (vitamin K-dependent protein). Although OC is a calcium-binding protein that is strongly expressed in bone, the effects of OC on bone remain obscure. However, a biomechanical analysis of the quality of the femora in OC-deficient mice showed that the yield energy (ductility of bone specimens), failure load (strength of the bone), and stiffness (elasticity of the bone) decreased dramatically after ovariectomy [20], suggesting that OC may have an important role in bone biology, and that OC deficiency may be associated with bone fragility. Thus, vitamin K may play an important role in maintaining bone health.

The present review revealed positive evidence for the effect of menatetrenone monotherapy on BMD and the incidence of fractures (mainly vertebral fractures) in postmenopausal women with osteoporosis. However, this evidence was derived from RCTs with small sample sizes. Thus, menatetrenone is used as a second-line medicine for the treatment of postmenopausal osteoporosis in Japan [8]. Knapen et al. [21] reported that menatetrenone (45 mg/day) improved hip bone geometry, bone strength indices, and bone mineral content in healthy postmenopausal women, supporting the effect of menatetrenone on bone health.

The mechanism whereby menatetrenone exerts its protective effect against fractures remains uncertain. Menatetrenone reduced the incidence of clinical fractures despite causing no significant change or only a modest increase in BMD. However, menatetrenone is capable of improving bone quality (material property) and preventing fractures. As noted above, impaired vitamin K nutritional status results in impaired γ-carboxylation of OC, and one possible explanation for its protective effect against fractures is that menatetrenone may promote γ-carboxylation of OC and induce the production and secretion of OC by osteoblasts. However, the vitamin K intake (500 μg/day) needed for full γ-carboxylation of OC may be approximately 100-fold lower than the dose of menatetrenone (45 mg/day) needed to produce a clinical effect [9].

The present review investigated the effect of an anti-osteoporotic medicine, menatetrenone (vitamin K2) on the skeleton in postmenopausal women with osteoporosis. However, vitamin K1 is also considered to contribute to bone health, because all vitamin K molecules are converted into menaquinone-4 (vitamin K2) [22] and then become active. So, the effects of vitamin K1 on bone parameters appear to be equivalent to those of vitamin K2. Cheung et al. [23] reported that vitamin K1 (5 mg/day) did not protect against age-related decline in BMD, but prevented clinical fractures in postmenopausal women with osteopenia. The World Health Organization has proposed a set of guidelines for the diagnosis of osteoporosis in adult women based on a measurement of BMD expressed as the number of SD below young adult mean (t-score); [24] osteopenia (low bone mass) is defined as BMD between 1 and 2.5 standard deviation (SD) below the mean value of peak bone mass in young normal women, while osteoporosis is defined as BMD more than 2.5 SD below the mean value of peak bone mass in young normal women [24]. The results of Cheung study appeared to be consistent with those of menatetrenone.

A small RCT showed the beneficial effects of combined menatetrenone and alendronate therapy on serum ucOC concentrations and femoral neck BMD in postmenopausal women with osteoporosis [19]. This result suggests the possibility that menatetrenone could serve as an adjuvant of bisphosphonates in the treatment of postmenopausal osteoporosis. However, it remains uncertain whether this combination therapy is more useful for preventing fractures than single therapy with bisphosphonates. Thus, menatetrenone appears to be a second-line medicine in postmenopausal women with osteoporosis [8].

The present review showed the effects of menatetrenone on serum ucOC concentrations, BMD, and fracture incidence in postmenopausal women with osteoporosis. The study subjects of eight RCT analyses did not always have higher serum ucOC concentrations. Therefore, it is not established whether menatetrenone is more effective for reducing fractures in postmenopausal osteoporotic women with higher serum ucOC concentration than those with lower serum ucOC concentrations, despite the fact that high serum ucOC concentrations are related to an increased risk for fractures in postmenopausal women with osteoporosis. Further studies are needed to clarify this issue.

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6. Conclusions

The present review revealed positive evidence for the effects of menatetrenone monotherapy on fracture incidence in postmenopausal women with osteoporosis. However, this evidence was derived from RCTs with small sample sizes. The efficacy of combined bisphosphonate and menatetrenone therapy against fractures compared with bisphosphonate monotherapy remains to be established. Currently, menatetrenone is a second-line medicine for the treatment of postmenopausal osteoporosis.

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Conflicts of Interest

The authors declare no conflict of interest.

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References

1. Hauschka P.V., Lian J.B., Cole D.E., Gundberg C.M. Osteocalcin and matrix Gla protein: Vitamin K-dependent proteins in bone. Physiol. Rev. 1989;69:990–1047.  [PubMed]

2. Koshihara Y., Hoshi K. Vitamin K2 enhances osteocalcin accumulation in the extracellular matrix of human osteoblasts in vitro. J. Bone Miner. Res. 1997;12:431–438. doi: 10.1359/jbmr.1997.12.3.431.  [PubMed] [Cross Ref]

3. Shearer M.J. Vitamin K. Lancet. 1995;345:229–234. doi: 10.1016/S0140-6736(95)90227-9.[PubMed] [Cross Ref]

4. Vermeer C., Jie K.S., Knapen M.H. Role of vitamin K in bone metabolism. Annu. Rev. Nutr. 1995;15:1–22. doi: 10.1146/annurev.nu.15.070195.000245.  [PubMed] [Cross Ref]

5. Tsugawa N., Shiraki M., Kamao M., Kamao M., Ozaki R., Tanaka K., Okano T. Usefulness of serum undercarboxylated osteocalcin measurement as a predictor for clinical fractures. Osteoporos. Jpn. 2010;18:254–256. (in Japanese)

6. Shiraki M., Yamazaki Y., Shiraki Y., Hosoi T., Tsugawa N., Okano T. High level of serum undercarboxylated osteocalcin in patients with incident fractures during bisphosphonate treatment. J. Bone Miner. Metab. 2010;28:578–584. doi: 10.1007/s00774-010-0167-2.  [PubMed] [Cross Ref]

7. Orimo H., Fujita T., Onomura T., Inoue T., Kushida K., Shiraki M. Clinical evaluation of soft capsule menatetrenone (Ea-0167) in the treatment of osteoporosis. Late Phase II Dose Study. J. New Rem. Clin. 1992;41:1249–1279. (in Japanese)

8. Orimo H., Nakamura T., Hosoi T., Iki M., Uenishi K., Endo N., Ohta H., Shiraki M., Sugimoto T., Suzuki T., et al. Japanese 2011 guidelines for prevention and treatment of osteoporosis-executive summary. Arch. Osteoporos. 2012;7:3–20. [PMC free article]  [PubMed]

9. Iwamoto J., Sato Y., Takeda T., Matsumoto H. High-dose vitamin K supplementation reduces fracture incidence in postmenopausal women: A review of the literature. Nutr. Res. 2009;29:221–228. doi: 10.1016/j.nutres.2009.03.012.  [PubMed] [Cross Ref]

10. Shiraki M., Shiraki Y., Aoki C., Miura M. Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis. J. Bone Miner. Res. 2000;15:515–521. doi: 10.1359/jbmr.2000.15.3.515.  [PubMed] [Cross Ref]

11. Iwamoto J., Takeda T., Ichimura S. Effect of menatetrenone on bone mineral density and incidence of vertebral fractures in postmenopausal women with osteoporosis: A comparison with the effect of etidronate. J. Orthop. Sci. 2001;6:487–492. doi: 10.1007/s007760100002.  [PubMed][Cross Ref]

12. Ishida Y., Kawai S. Comparative efficacy of hormone replacement therapy, etidronate, calcitonin, alfacalcidol, and vitamin K in postmenopausal women with osteoporosis: The Yamaguchi Osteoporosis Prevention Study. Am. J. Med. 2004;117:549–555. doi: 10.1016/j.amjmed.2004.05.019.[PubMed] [Cross Ref]

13. Inoue T., Fujita T., Kishimoto H., Makino T., Nakamura T., Nakamura T., Sato T., Yamazaki K. Randomized controlled study on the prevention of osteoporotic fractures (OF Study): A phase IV clinical study of 15-mg menatetrenone capsules. J. Bone Miner. Metab. 2009;27:66–75. doi: 10.1007/s00774-008-0008-8.  [PubMed] [Cross Ref]

Freaky

A wild animal has been coming to the doorstep at night looking for goodies.  I discovered that my mother was feeding him, and lectured her sternly.  Number one, he is undoubtedly rabid and we will all die.  Before we succumb to rabies we will have several other dread diseases, plus who knows what else.  We will also be attacked.  Moreover, what sort of animal is this?  I told her she was encouraging rodents.  She kept insisting it was a possum.  "How do you know that?'  "I've seen him."  "Do you know what a mess he makes?  He'll bring all his friends, too."  

There was no stopping her, and finally I said, "OK, feed your freaky little pet."  She therefore named him Freaky.  

Freaky has been cautious enough that I really didn't believe in Freaky.   But day after day goodies and table scraps disappeared at the backdoor.   

Tonight I put out part of a salad for Freaky, and later decided to put out a bite of hamburger.  When I opened the backdoor, I heard a rustling, and thought the cat was at the door.  No, it was Freaky boldly eating goodies.  I was surprised that he didn't run when he saw me, but he was too intent on his goodies.  Freaky is definitely a possum. 

Something wonderful has happened to my blood pressure

I've have racked my brains over my blood pressure.  Up until around ten years ago, it tended too run low.  Then suddenly it began to become to high.  The next thing you know I was hearing about taking blood pressure medication. N O NO.  

"Well, what's your plan?" the doctor would say.  "Diet. Exercise. Niacin supplements.  I don't know."  

The doctor sent me home with a blood pressure monitor, and even set me up on a program whereby I was called in the morning and asked if I had checked my blood pressure and what it was.  At the time I had decided to go on a fast, and every morning it would be about 105/70.  What??  

But eventually I would eat and be back at the doctor's office with blood pressure of 160/95.  I insisted this only happened at the doctor's office because of white coat syndrome.  A nurse in a purposefully green jacket saw my alarm and asked, "Are you afraid of me?"  "Yes."  "????"  Well, patients check in but they don't check out. 

And so the days went by, and I heard horror stories of what happened to bad patients with high blood pressure.  I even met some of them.  One man in the waiting room said that he had had kidney failure from high blood pressure.  He was 45 and now on dialysis.  I really didn't know what to do.  Besides that, I read that people taking blood pressure medicine may decrease their risk of stroke, but not of heat attack.  I was doomed.  This just wasn't going well.  

And it seemed like I was being blamed.  Since I didn't know what to do, I hoped for the best.  

Then a couple of weeks ago I read that most people are deficient in Vitamin K2, which regulates blood calcium.  A deficiency would cause atherosclerosis.   Up to that time I had thought that the solution for that was green leafy vegetables.  Why did I think that?  Well, I was told that by doctors.  "Vitamin K is in green leafy vegetables," they said.  If you google that right now, and ask, what food contain Vitamin K2, you will find medical university sites that will tell you to eat plenty of green leafy vegetables to get Vitamin K2.

How much Vitamin K2 would be in cabbage, kale, spinach, etc?  None.  NONE.  The only vegetable source of Vitamin K2 is natto. People don't eat that around here.  

What seems to have happened is that I began to go to the doctor and be encouraged to take calcium, especially since I'm female.  Then a few years ago I was tested for Vitamin D and was surprisingly deficient.  So I took Vitamin D and calcium.  

But then without adequate K2, the calcium does not build bones but  winds up in the arteries and other places, like kidneys.  

Therefore, when I heard about this, I began taking Vitamin K2 and wondered what was going on in doctor land.  Watching videos on this, there is even one famous physician arguing of the dangers of taking K2 since he believed that reducing the calcium in the blood would cause the plaque in the arteries not to harden, and that would make it more dangerous.  I think this was a case of overthinking.  Or possibly discovering that evidence has proved a long held tenet wrong and trying to justify it.  Another video was of a doctor touting taking Vitamin D and "Vitamin K," which is what has led to all the confusion in the first place.  Vitamin K1 and Vitamin K2 are totally different things.   Vitamin K2 should be taken with Vitamin D.  

So I've been taking Vitamin K2.  Then a thought occurred to me.  Maybe this had affected my blood pressure.  

For the first time in a long time my blood pressure was down to normal levels.  Yay!  

What foods contain K2?  Meat, cheese and eggs.  And natto. But I did eat an abundant amount of meat, cheese and eggs.  I have even been criticized for that.  It seems that modern methods of farming have depleted K2 from these food sources.  Are supplements a must?  Well, I think if you're taking calcium and Vitamin D, yes, you should also supplement with K2.  And considering that at least 80% of the population has a deficiency of K2, it would seem like a good thing to do. 

And that's my story.