Lipids for the Prostate, Part 1

In April this year, the daughter of a 70 y/o man with prostate cancer emailed us. She reported her father, KG, had long-standing prostate enlargement which had been monitored closely. Then in November 2020, now a year ago, his PSA and alkaline phosphatase were markedly elevated - his PSA was 940 (over 4 is high) and his alkaline phosphatase 971(over 126 is high). This elevation in alk phos is the result of extensive bone metastases seen on his scan. KG’s only other significant medical history is a stint, placed in 2018. Starting with the stint, he is prescribed BP lowering medications, a statin and Atenolol. Lipid-bound Selenium, LbSe, was recommended in April, one dropper approximately every 12 hours. This dropper can be placed directly in the mouth, on bites of food or in the large end of a double 00 gelatin capsule. Why LbSe? A simultaneous serum and red-blood-cell potassium, 4.3 and 94 respectively, indicates he is anabolic at the cell level.  In anabolism, there is relatively more potassium inside cells compared to serum.  In other words, there is an extra- to intracellular shift in potassium. Our man’s serum potassium is below 4.5 and his red-blood-cell potassium, RBC K, is greater than 90, indications he is anabolic on the cell level.1 LbSe is catabolic on the cell level.  Further, his bone scan showed lucent bone lesions. Lucent bone is less dense bone. Lucent bone lesions are anabolic lesions. Anabolic bone lesions are osteolytic, that is, bone is dissolved. Descriptions of bone metastases on scan reports are extremely valuable and reliable. The scans of a woman with breast cancer and bone metastases this year specifically describe lytic lesions and “lytic destruction”. Although she is not able to get a RBC K, these scans are definitive for an anabolic off-balance in cells. She is responding positively to LbSe. LbSe for KG yes, starting in April, and Lipid-bound Calcium, LbCa, was added a month later. Both are catabolic at the cell level. I chose LbCa also because his serum calcium was low, at 8.6. Since approximately one third of serum calcium is bound to albumin, a low albumin will decrease serum calcium. Therefore, it is important to note his albumin was normal at that time.  Dr. Revici found that the inability of anabolic cancers to utilize calcium favors their metastases. There is much more to say about LbCa that we will cover in another podcast.  When KG began LbSe in April, his alk phos had already decreased from last November’s 971 to 670. He had received two injections at the beginning of this year that decrease testosterone by antagonizing gonadotrophin-releasing hormones LH and FSH.  Additionally, he took an androgen synthesis inhibitor daily and a monoclonal antibody used for bone metastases monthly. Actually, KG’s drop in PSA was more dramatic than that of his alk phos. His PSA of 940 a year ago dropped to 21 per a test in May.  Then, on his August 30th lab, his alk phos and PSA are both normal!! We are all surprised, especially his urologist and oncologist. A decrease was expected, yes, but slowly, not precipitously and certainly not to normal. Words of caution are warranted: we have never witnessed improvements in actual tumors from LbSe as described here for bone metastases, even when an extra- to intracellular shift of potassium has been documented. Since LbSe is used for cancers in conjunction with other therapies, improvements must be attributed to the protocol, not specifically to LbSe. Likewise, KG received medications aimed at reducing his cancer. How does LbSe work? LbSe oxidizes leukotrienes, LTRs. LTRs are metabolites of arachidonic acid, AA. Dr. Revici identified a fatty acid in the 1930’s with three parallel double bonds that causes irreversible damage. Other pro-inflammatory fatty acids do not. Appropriately, Dr. Revici called them conjugated trienic fatty acids. ..continued