The effect on mitochondrial dna is complex. The causes of death are many but the telomere count is a slow march towards death. Reduced telomeres have shown links to effects than cause death.

For humans, the length of the remaining telomere is usually an indicator of how many divisions a dividing cell has left. One study found an inverse relationship between telomere length and pulse pressure, indicating a possible direct relationship between vascular aging and telomere length [HYPERTENSION; Jeanclos,E; 36(2):195-200 (2000)]. Higher levels of oxidative stress increase the rate of telomere shortening [TRENDS IN BIOCHEMICAL SCIENCES 27(7):339-344 (2002)]. Once the telomere is gone, functional genetic DNA would be lost with each cell division. Prior to complete erosion of the telomere a signal is sent to p53 protein (possibly by ATM protein) to stop the cell cycle causing the cell to go into a slow-decaying, non-replicative state known as replicative senescence. Telomeres protect chromosomes like the plastic cap that prevents shoe-laces from becoming frayed at the ends. Telomeres have been shown to be seven times more vulnerable to hydroxyl radical oxidation than similar-sized DNA control fragments, indicating that telomeres could sacrificially protect coding DNA from oxidative damage [JOURNAL OF BIOLOGICAL CHEMISTRY; Henle,ES; 274(2):962-971 (1999)].

Telomere ComplexTelomere Complex

Telomeres are actually a loop-like structure which is associated with an assortment of proteins, the most notable of which are the Telomeric Repeat-binding Factors (TRFs). TRF1 regulates telomere length, assisting the telomerase enzyme. TRF2 models the telomere into the T−loop structure. TRF2 may be protecting the single-stranded 3'−end overhang from degradation, and by binding to ATM prevents the ATM-dependent DNA damage response [THE EMBO JOURNAL; Blasco,MA; 24(6):1095-1103 (2005)]. Loss of TRF2 from telomeres directly signals apoptosis [SCIENCE; Karlseder,J; 283:1321-1325 (1999)]. TRF2 stimulates the helicase activity of both WRN (of Werner's Syndrome) and BLM (of Bloom Syndrome), which may play a role in telomere maintenance [JOURNAL OF BIOLOGICAL CHEMISTRY; Opresko,PL; 277(43):41110-41119 (2002)]. Ku proteins (normally active in double-strand break repair) prevent aberrant telomere-telomere fusions. Tankyrase is a PARP — Poly (Adenosine diphosphate-Ribose) Polymerase — which can ADP-ribosylate TRF1, thereby removing it from DNA and allowing telomerase lengthening of the telomere [SCIENCE; Pirrotta,V; 299:528-529 (2003)]. TRF2 is regulated by PARP−2 [MOLECULAR AND CELLULAR BIOLOGY; Dantzer,F; 24(4):1595-1607 (2004)].

Germ cells, stem cells and "immortalized" cancer cells contain an enzyme called telomerase that replaces lost telomeres, thus preventing them from experiencing a Hayflick Limit. Telomerase is a reverse transcriptase, meaning an enzyme that makes DNA from an RNA template (the reverse of normal transcription which uses DNA as the template for making RNA). In human germ cells or 85% of cancer cells human TElomerase Reverse Transcriptase (hTERT) and an RNA template are sufficient conditions for the creation of new telomeres. Because most cells normally express the RNA template, derepression of hTERT is the critical step for acquiring telomerase activity. Defects in proteins required to maintain telomere function can also lead to chromosome instability and cancer [EXPERIMENTAL GERONTOLOGY 36:1619-1637 (2001)]. Telomerase expression can actually make cells more resistant to apoptosis induced by oxidative stress [FEBS LETTERS; Ren,J; 488:133-138 (2001)].

Digesting food takes a lot of energy. Eating less food means your body does not have to work as hard.

I saw a man on a new show the other day who stated that our bodies are designed to feed off of the stored fat we have. He said that delaying breakfast is not a bad thing.

I know when I eat less, I actually feel more energetic and when I have eaten a large meal, I just want to take a nap while my body has to work digesting the food.

...then there are people who claim that you can go without eating food and get your energy from the earth and the sun.

Human stem cell producing leukocyte with shortened telomeres has no impact on the function of new cells according to studies.
Many studies in fact show that expression of telomerase in somatic cells or the supplement of telomerase increases incidences of cancer. Cellular senescence is a defense mechanism trigger after about 60 divisions (Hayflict limit) is accommodates for the oxidative stress which as you pointed out is rather complex nevertheless, without the trigger triggered cellular senescence, damaged cells are more likely to have mutations that become cancerous that would have otherwise stopped developing and destroyed. While telomere shortening does pose a problem in the long run, human stem cells are able to function well into a person's normal life. These stem cells determine the functionality of their specific cells so stem cells in good order will produce good specific cells.

This has been shown in the stem cells of old patients which does not appear to work as well as young people's stem cells. Rather it isn't the number of stem cells that decrease (in some cases it increases) although it is tissue dependent but functionality changes. There is a loss of homeostasis and as a result, the stem cell produce different ratios of progenitors resulting in a different ratio of specific offspring.

Oddly, when the stem cell of an old patient is transplanted into a younger patient, homeostasis is restored which is attributed to the SC Niche, a group of cells housing the Stem Cell which sends signals on when to divide and what to divide into. The "old" stem cell behaves like new again despite having a shorter telomere and the accumulation of DNA damage due to oxidation.
In other words, telomere shortening isn't a problem in one life span. Perhaps 2 or 3 but it isn't a problem within the first 100 years.

The decrease in lifespan due to telomere shortening as only been been in the lab with the telomeres of stem cell being forced to reduce and is uncharacteristic of normal aging.

It can't necessarily be extended to far more complex organisms as humans in such a simple assertion. Anti-oxidants such as vitamin C, Vitamin E, and CoQ-10 have been shown to increase the lifespan of short lived mice such as the UCadiz mice, but has no effect whatsoever on long lived mice. Evidence of reduced longevity asserted in an experiment involving a genetic mutation resulting in the elimination of telomere isn't enough to account for the lifespan observed in nature ex with mice that die naturally (whose telomeres are in good health and die by some other means)