The Sphenoid
News You Need To Know - Cholesterol

Dr. James Cross
July 2016

Over the last 30 years or so there has been much reported about the damaging effect of cholesterol on our health, in particular the cardiovascular system. Supposedly cholesterol is the evil substance that is directly responsible for heart attacks and arterial blockage. We have been told repeatedly how important it is to reduce cholesterol as much as possible and if we do this the incidence of heart disease will drop dramatically. So, let’s look at the actual facts and see if this is accurate.

The following are two lists of the benefits of cholesterol and the dangers of cholesterol that is too high.


-        Covers the nerves in protective coating

-        Is the base substance for vitamin D production (please see the attached list of vitamin D


-        Provides for repair of all cell membranes and cell walls in the body

-        Is necessary for proper immune function

-        Necessary for muscle strength

-        Used by the body to produce bile for digesting fats and to neutralize acid from the stomach when the acidic food enters the small intestine

-        60-75% of the brain is cholesterol

-        Cholesterol is the base from which all steroid hormones are produced (testosterone, estrogen, progesterone)



-        Cholesterol forms part of the plaque that blocks arteries (the remaining materials are fibrin, platelets and calcium)



-        Lowers cholesterol and recently felt to reduce chronic inflammation– THAT’S IT FOLKS! NOW WE WILL CONSIDER IF THIS IS TRULY A BENEFIT!!



-        FATIGUE(1)                             

-        LOSS OF STRENGTH(2)





-        CATARACTS   (9)


-        LIVER DAMAGE    (14)




“But my doctor says the statin drug will decrease the risk of a heart attack or stroke!” (21) Well, the journal Atherosclerosis  (17)published a study that showed that statin use was associated with a 52% increased prevalence of calcified coronary arteries compared to non-users. The reason for this is statin drugs block the production of vitamin K2 (menaquinone) (19,22,23,24). Menaquinone helps keep calcium in the bones and out of soft tissues – including the arteries. It is interesting to note that statin drugs function by blocking CoQ10 enzyme that is necessary for energy production in the mitochondria in all our body cells. The heart, because it beats 24-7, has about 200 more times mitochondria than skeletal muscle and therefore needs about 200 more times CoQ10. Think that might be a problem? In 2009 a study published in the Journal of Clinical Cardiology found that the use of statin medications resulted in decreased cardiac function.


One last study about the cardiovascular system I would like to cite is the Jupiter Study (18,20)that concluded that the use of a statin medication reduced the likelihood of a cardiovascular event (heart attack or stroke) by 50%. The raw data show that if a person used a statin drug the likelihood of a cardiovascular event not happening was 98.4%. If no statin drug was used the likelihood of a cardiovascular event not occurring was 97.2%. The difference 2.8%-1.6% or 1.2% difference. Yes, this is 50% less, but is it significant’? It’s 1.2%! In exchange for this 1.2 % you risk all of the side effects associated with statin medication. You decide.


And finally, how about Parkinson’s Disease. A study in the Journal of Movement Disorders found that the use of statin medication increased the risk for developing Parkinson’s Disease.  (5)


There is a great deal more information concerning cholesterol, statin drugs and heart disease, but this should give you enough information for you to decide on how you want to approach the subject.


Now, I am not suggesting you discontinue any medication that your doctor has prescribed. I am simply informing you about the benefits and risks of using statin medications. If you are concerned about side effects of any medication, you should always discuss your concerns with the doctor who prescribed the medication.


If you are interested in learning what your actual risk factors are for cardiovascular problems, I suggest the following blood tests:

-        Cholesterol panel to look for the amount of HDL cholesterol and the risk ratio of HDL to total cholesterol and triglyceride (an increasingly important risk factor)

-        A1C to test for your 3 month average glucose

-        Homocysteine, an aggressive amino acid that can damage blood vessels and create inflammation

-        CRP-hs; this measures the degree of inflammation particularly in your cardiovascular system


1.      Golomb, Beatrice A., M.D., PhD, Evans, Marcella A., B.S., Dimsdale, Joel E., M.D., and White, Halbert L., PhD.

Effects of Statins on Energy and Fatigue with Exertion: Results From a Randomized Controlled Trial. Archives of Internal  Medicine 2012 Aug. 13; 172(150: 1180-1182.

2.      Mygland, A., Ljostad, U., Krossnes, BK. Persisting weakness after withdrawal of a statin. BMJ Case Report 2014 Apr 8; pii: bcr2013203094. doi: 10.1136/bcr-2013-203094

3.      Jamolowicz, Al, Chen, HY, Panegyres, PK. Statins and memory loss: An Australian experience. Australian Medical J. 2015 Mar 31;8(3): 73-9. doi: 10.4066/AMJ. 2015.2014. eCollection 2015.

4.      Tierney, EF, Thurman, DJ, Beckles, GL, Cadwell, BL. Association of statin use with peripheral neuropathy in the U.S. population 40 years of age or older. J Diabetes 2013Jun;5(2):207-15. Doi: 10.1111/1753-0407.12013.

5.      Huang, X, Alonso, A, Guo, X, Umbach, DM, Lichtenstein, ML, Ballantyne, CM, Mailman, RB, Mosley, TH, Chen, H. Statins, plasma cholesterol, and risk of Parkinson’s disease: a prospective study. Movement Disorders, 2015 Apr, 30(4):552-9. Doi: 10.1002/mds. 26152. Epub 2015 Jan 14.


6.      Bergua, C, Chiavelli, H, Simon, JP, Boyer, O, Jouen, F, Stenzel, W, Martinet, J. Immune-mediated necrotizing myopathy. Z. Rheumatology 2016 Mar;75(2):151-156


7.      Ghittoni,R, Patrussi, L, Pirozzi, K, Pellegrini, M, Lazzerini, PE, Capecchi, Pl, Pasini, FL, Baldari, CT. Simvastatin inhibits T-cell activation by selectively impairing the function of Ra Superfamily GTPases. FASEB J. 2005 Apr;19(6):605-7. Epub 2005 Jan 27.


8.      Holder, K. Myalgias and Myopathies: Drug-Induced Myalgias and Myopathies. FP Essent 2016 Jan; 440:23-7.


9.      Leuschen, J et al. Association of statin use with cataracts: a propensity score-matched analysis. JAMA Ophthalmology 2013.


10.   Lorza-Gil, E, Salerno, AG, Wanschel, AC, Vettorazzi, JF, Ferreira, MS, Rentz, T, Catarino, RR, Oliveira, HC. Chronic use of pravastatin reduces insulin exocytosis and increases B-cell death in hypercholesterolemic mice. Toxicology 2016 Feb 17;344-346:42-52. Doi: 10.1016/j. tox. 2015.12.007.


11.   Katriski, N, Athyros, VG, Karagiannis, A, Mikhailidis, DP. Statins and Type 2 Diabetes Mellitus: An Update After 1 Year. Curr Pharm Des 2016 Jan 24.


12.   About 150 authors and co-authors – I am not going to list them; they are on the paper I have in my office in case you are interested. HMG-coenzyme A reductase inhibition, type 2 diabetes, and bodyweight: evidence from genetic analysis and randomised trials. Lancet 2015 Jan 24; 385(9965):351-361. Doi: 10.1016/So140-6736(14)61183-1.


13.   Tseng, CH, Diabetes b ut not insulin increases the risk of lung cancer: a Taiwanese population-based study. PLoSOne 2014 Jul 3;9(7):e101553,doi:10.137/journal. Pone.0101553.


14.   Bjornsson, E, Jacobsen, EI, Kalaitzakis, E. Hepatotoxicity associated with statins: reports of idiosyncratic liver injury post-marketing. J. Hepatology 2012 Feb;56(2):374-80.doi: 10.1016/j.jhep.2011.07.023.


15.   Chang, CC, Ho,SC, Chiu,HF, Yang, CY. Statins increase the risk of prostate cancer a population-based case-control study. Prostate 2011 Dec; 71(16)1818-24. Doi 10.1002/pros.201401.


16.   Huang, CY, Chung, SD, Kao, LT, Lin, HC, Wang, LH. Statin Use Is Associated with Bladder Pain Syndrome/Interstitial Cystitis: A population-Based Case-Control Study. Urology Int. 2015;95(2):227-32. Doi:10.1159/000431185.


17.   27 authors, I am not going to list them; they are available in my office on the copy of this paper. Statin use and coronary artery plaque composition: results from the International Multicenter CONFIRM Registry. Atherosclerosis 2012 Nov; 225(1): 148-53.doi:10.1016/j.atherosclerosis. 2012.08.002.


18.   deLongeril, M, Salen, P, Abramson, J, Dodin, Hamazaki, T, Kostucki, W, Okuryama, H, Pavy, B, Rabaeus, M. Cholesterol lowering, cardiovascular diseases, and the rosuvastatin-JUPITERcontroversy: a critical reappraisal. Arch Inter Med 2010 Jun 28l170(12):1032-6.doi: 10.1001/archinternalmed.2010.184.


19.   Okuyama, H, Lansjoen, PH, Hamazaki, T, Ogushi, Y, Hama,R, Kobayashi, T, Uchino, H. Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms. Expert Rev Clin Pharmalol. 2015 Marl 8(2):189-99.doi. 10.1586/17512433.2015.1011125.


20.   Seaman, D, D.C. Statins and Cardiovascular Disease: Not as Protective as We’re Led to Believe: A review of the JUPITOR study, Dynamic Chiropractic newspaper article.


21.   Diamond, DM, Ravnskov, U. How statistical decep0tion created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease. Expert Rev Clin Pharmacol. 2015 Mar: 8(2):201-10.doi: 10.1586/17512433,2015.1012494.


22.   Yoshida, M, Jacques, PF, Meigs, JB, Saltzman, E, Shea, MK, Gundberg, C, Dawson-Hughes, B, Dallal, G, Booth, SL.

Effect of vitamin K supplementation on insulin resistance in older men and women. Diabetes Care. 2008 Nov:31(11):2092-6. Doi: 10.2337/dc08-1204.


23.   Hyung Jin Choi, MD, Juyoun, Yu, BS, Hosanna, Choi, BS, Jee Hyun, An, MD, Sang Wan, Kim, MD, PhD, Kyong Soo, Park, MD, PhD, Hak C, Jangm MD, PhD, Seong Yeon, Kim, MD, PhD, Chan Soo, Shin, MD, PhD. Vitamin K Supplementation Improves Insulin Sensitivity via Osteocalcin Metabolism: A Placebo-Controlled Trial. Dept of Internal Medicine, Seoul National U. College of Medicine, Seoul, South Korea.


24.   Gast, GC, deRoos, NM, Sluijs, I, Bots, ML, Beulens, JW, Geleijnse, JM, Witteman, JC, Grobbee, DE, Peeters, PH, van der Schouw, YT. A high menaquinone intake reduces the incidence of coronary heart disease. Nutr Metab Cardiovasc Dis. 2009 Sep; 19(7):504-10. Doi: 10.1016/j.numecd.2008.10.004.

The Sphenoid

By Jack Dolbin, DC, CSCS
January, 2016

“Continuous treatment of the musculoskeletal system without addressing the craniosacral dysfunction will lead to less than satisfying results.”

This statement by Dr. Philip Greenman DO FICO, Professor of biomechanics Michigan State University School of Osteopathic Medicine got my attention for a couple reasons. Principally because of the respect I had for Dr. Greenman, the author of two books and numerous research articles on the efficacy of manual medicine and a leader in his field. This encouraged me to take a few courses from the Upledger Institute on the topic of Craniosacral Therapies. While I found the principles compelling and the outcomes very good, I didn’t feel I could incorporate it into my arsenal of therapies. The time involved in the application of the therapy made it unworkable in my practice. That all changed as I read Dr. Jerry Tennent’s book “ Healing is Voltage”. In his chapter on the “ Bowling Ball Syndrome” I was introduced to a treatment protocol that was both defensible scientifically and could be applied in a time effective manner. Simply put the treatment released the compression of the Sphenobasilar junction thus releasing the entire cranial mechanism.

Craniosacral Therapy can be traced back to the work of Dr. William G. Sutherland DO. Dr. Sutherland, after years of study and the application and experimentation developed aconcept that integrated the Skull, meningies, brain, spinal cord, and sacrum into a function unit based on the concept that the cranial bones are dynamic and move in relation to the inhalation/exhalation activating force. This dynamic movement drives cerebrospinal fluid from the third and fourth ventricles through the subarachnoid space providing nutrition to the brain, spinal cord and nerves, a key to maximum neurological function. Sutherland hypothesized that the skull would have normal mobility during health and show restrictions in response to trauma and disease. This theory, like many, was met with criticism. The main objection being that cranial sutures fuse in about the second year of life and thus are not dynamic. However, continued research along with more sophisticated imaging has demonstrated that these sutures are open into the eight decade of life. Additional criticism is the lack of intertester reliability in evaluating fixations in the sutures.

Enter two men, an Osteopath Dr.Robert  Boyd and a Chiropractor  Dr.Doug Hayes. These physicians developed a method of evaluation and correction that is both effective and time friendly in a busy practice. Their focus is on the spheniobasilar junction as the main articulation in the movement of cranial bones. The sphenoid bone is called the keystone of the entire cranial mechanism. Fixations in the sphenoid will compress all the bones just as the keystone in early architecture will compress all the stones in the arch. Conversely, releasing the sphenobasilar articulation will decompress the entire cranial mechanism allowing for the dynamic pumping of the cerebrospinal fluid and recentering the foramen magnum and C1,C2.

In my practice I have been applying these techniques along with my manual chiropractic spinal, extremity, and visceral adjusting. My outcomes have improved dramatically.

In our seminars at Fetterman Events we go into the evaluation and application of this technique along with the science behind the principle.